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Cadmium(II) is an omnipresent environmental toxicant emitted from various industrial sources and by anthropogenic sources such as smoking. Cadmium(II) enters our body through various sources including contaminated food and drinks and from active or passive smoking. It spares no organs in our body and the calamities it invites include primarily nephrotoxicity, osteotoxicity, teratogenicity, endocrine disruption, hepatotoxicity and carcinogenicity above all. It brings about a bolt from the blue in the cellular biochemistry by generating reactive oxygen species (ROS), disrupting the factors involved in the repair of DNA lesions and many other toxic nuisances otherwise by modulating the cell signalling machinery and acting as a potent carcinogen above all. In this review, we have tried to decipher some of the mechanisms played by cadmium(II) in exhibiting its toxic effects on various system of our body.

Fetal development of the mammalian testis relies on a series of interrelated cellular processes: commitment of somatic progenitor cells to Sertoli and Leydig cell fate, migration of endothelial cells and Sertoli cells, differentiation of germ cells, deposition of the basement membrane, and establishment of cell–cell contacts, including Sertoli–Sertoli and Sertoli–germ cell contacts. These processes are orchestrated by intracellular, endocrine, and paracrine signaling processes. Because of this complexity, testis development can be disrupted by a variety of environmental toxicants. The toxicity of phthalic acid esters (phthalates) on the fetal testis has been the subject of extensive research for two decades, and phthalates have become an archetypal fetal testis toxicant. Phthalates disrupt the seminiferous cord formation and maturation, Sertoli cell function, biosynthesis of testosterone in Leydig cells, and impair germ cell survival and development, producing characteristic multinucleated germ cells. However, the mechanisms responsible for these effects are not fully understood. This review describes current knowledge of the adverse effects of phthalates on the fetal testis and their associated windows of sensitivity, and compares and contrasts the mechanisms by which toxicants of current interest, bisphenol A and its replacements, analgesics, and perfluorinated alkyl substances, alter testicular developmental processes. Working toward a better understanding of the molecular mechanisms responsible for phthalate toxicity will be critical for understanding the long-term impacts of environmental chemicals and pharmaceuticals on human reproductive health.

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates the toxicity of halogenated and polycyclic aromatic hydrocarbons in vertebrates. Thus, increased knowledge of AhR-mediated responses to xenobiotics is imperative. Sebastes schlegelii is increasingly being used as a model for studying environmental toxicology; hence, in this study, the presence of AhR2 was evaluated in S. schlegelii. The results showed that the predicted AhR2 amino acid sequence contained regions characteristic of other vertebrate AhRs, including the basic helix-loop-helix and PER-ARNT-SIM domains in the N-terminal half, but it had minor similarity with other vertebrate AhRs across the C-terminal half; it did not contain the distinct glutamine-rich domains found in mammalian AhR2. Phylogenetic analysis demonstrated that S. schlegelii AhR2 was clustered within the teleost AhR2 branch. Additionally, AhR2 mRNA was detectable in all 11 tissues tested, with the highest mRNA levels in the heart, pyloric ceca, and liver. Furthermore, exposure to the AhR agonists showed that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 μg/g body weight) induced a significantly higher increases in AhR2 expression in the gills, liver, kidneys, and spleen in 48 h than benzo[a]pyrene (2 μg/g body weight), and β-naphthoflavone (50-μg/g body weight); AhR2 mRNA levels upon TCDD exposure were up-regulated by 16- and 10-fold in the gills and liver, respectively. These findings indicated that AhR was a highly sensitive receptor against TCDD. Thus, investigating AhR2 expression in the presence of other xenobiotics might offer further information for the elucidation of its crucial role in mediating toxicant metabolism in S. schlegelii.

The ongoing use of 1080 toxin for the control of mammal pests in New Zealand remains highly contentious. Several reviews over the last 25 years identified information gaps and areas of concern, bot...

In the search for biopesticides, increasing attempts have been made to obtain bioactive compounds from plants. In this regard, the insecticidal activity and deterrence of saponins obtained from Yucca schidigera Roezl(Agavaceae) were tested on the major stored product pest, Tribolium castaneum (Herbst) (Coleoptera :Tenebrionidae) via feeding bioassay. Adult beetles were reared on wheat grain dusted with saponins at 1 to 5% concentrations (wt/wt) for 1 to 14 days under optimal development conditions. Our results indicated that the increase of concentration and exposure periods enhanced mortality. The mortality reached 81 and 94% at 1 and 5% saponins, respectively, after 14d of exposure. In the choice test with treated and untreated grains, yucca saponins were able to deter adults immediately after the first 2hr up to the end of the exposure interval after 24hr at 1 and 5% concentrations. The respective deterrent indices were (0.43 - 0.55) and (0.52- 0.78) at the tested intervals. In addition, cellular immune reactions were recorded in adult females as shown by changes in the differential hemocyte counts (DHCs) following the challenge with yucca saponins for 72hr. Finally, the application of yucca saponins at 1 and 5% extensively reduced the grain damage potential by 70 and 80%, respectively, after 7d of application while the reduction increased after 14 d to 73% and 85%, respectively. Due to the combined contact, toxicant and deterrent properties of yucca saponins, they could be considered as a potentially applicable grain protectant against T. castaneum.

Methylmercury (MeHg) is a developmental toxicant capable of eliciting neurocognitive and neuromuscular deficits in children with in utero exposure. Previous research in Drosophila melanogaster uncovered that developmental MeHg exposure simultaneously targets the developing musculature and innervating motor neuron in the embryo, along with identifying Drosophila neuroligin 1 (nlg1) as a gene associated with developmental MeHg sensitivity. Nlg1 and its transsynaptic partner neurexin 1 (Nrx1) are critical for axonal arborization and NMJ maturation. We investigated the effects of MeHg exposure on indirect flight muscle (IFM) morphogenesis, innervation, and function via flight assays and monitored the expression of NMJ-associated genes to characterize the role of Nlg1 mediating the neuromuscular toxicity of MeHg. Developmental MeHg exposure reduced the innervation of the IFMs, which corresponded with reduced flight ability. In addition, nlg1 expression was selectively reduced during early metamorphosis, whereas a subsequent increase was observed in other NMJ-associated genes, including nrx1, in late metamorphosis. Developmental MeHg exposure also resulted in persistent reduced expression of most nlg and nrx genes during the first 11 days of adulthood. Transgenic modulation of nlg1 and nrx1 revealed that developing muscle is particularly sensitive to nlg1 levels, especially during the 20–36-h window of metamorphosis with reduced nlg1 expression resulting in adult flight deficits. Muscle-specific overexpression of nlg1 partially rescued MeHg-induced deficits in eclosion and flight. We identified Nlg1 as a muscle-specific, NMJ structural component that can mediate MeHg neuromuscular toxicity resulting from early life exposure.

We previously extracted and purified a chromene amide from Amyris texana and found this scaffold is moderately insecticidal and thus, this study aimed to test the insecticidal properties of 13 synthetically derived chromene analogs to the fall armyworm (FAW, Spodoptera frugiperda). Microinjection of chromenes with alcohol or aldehydes substitutions at the meta position on the benzopyran moiety led to moderate toxicity that was approximately 2- to 3-fold less toxic when compared to permethrin, yet microinjection of differently substituted chromenes exhibited little to no toxicity. Similarly, chromenes with alcohol or aldehydes substitutions at the meta position on the benzopyran moiety were among the most toxic chromenes studied through ingested exposure. In addition to acute toxicity, select chromenes significantly increased the percentage of developmental defects upon eclosion that prevented adult moths from being capable of flight, suggesting these compounds alter development. Interestingly, microinjection yielded differing signs of intoxication between alcohol and aldehyde substitutions where the alcohol resulted in flaccid paralysis and lethargy whereas aldehyde led to tonic contractions and hyperactivity. These contrasting signs of intoxication were also observed in electrophysiological assays where alcohol substitutions led to the depression of central neuron firing activity and aldehyde substitutions led to hyperexcitation of central neurons. In summary, the chromene amides led to acute lethality and/or altered developmental trajectories of FAW, yet the high doses required for acute mortality suggest these scaffolds hold relatively little promise for development into FAW-directed insecticides but may represent novel growth regulators for FAW.

Immune system is the adaptive defense mechanism which is evolved in vertebrates to keep them from invading pathogenic microorganisms and cancer. In immune system consists of some specialized cells like: lymphocytes, neutrophils, NK cells, basophils, macrophages, eiosinophils, mast cells, etc.Ecotoxicology is a subdisicipline of environmental toxicology concerd with studing the damaging effects of toxicants at the population and nature. Environmental toxicants are simply toxic substances in the nature. Environmental toxicant which is effect on ecosystem very badly.In this paper we discuss that how environmental toxicant effect on immune system or immune cells.

The influence of different concentrations of ions of copper, zinc, nickel, manganese of the aquatic environment on the ecotoxicological indicators of the wide range and the most numerous species of malacofauna of Ukraine – Planorbarius corneus (Linnaeus, 1758) was studied. According to the level of toxic effect on the coils, the pollutants studied by us belong to the categories of low-toxic (Mn 2+ ), moderately toxic (Ni 2+ ), highly toxic (Zn 2+ ) and highly toxic (Cu 2+ ) substances. The values of subthreshold, sublethal, chronically lethal, and acute lethal concentrations for each of the used toxicants (mg/dm 3 ) were determined according to the peculiarities of behavior and physiological condition of the experimental animals. As the concentrations of metal ions in the medium increase, the values of the latent period in P. corneus increase. The first signs of poisoning in animals are a weakening of motor activity and increased mucus secretion. At lethal concentrations (LC 100 ) of these toxicants in experimental mollusks develops a rapid pathological process. By the end of the experiment, all individuals in this group die. With increasing concentrations of heavy metal ions, lethal time and lethal mean time decrease. The highest lethal time values were observed for manganese (II) ions, and the lowest for copper ions. The reversibility of mollusk poisoning by different concentrations of these metals was studied. Restoration of functions in the studied animals is carried out in reverse order. Under the action of the same concentrations of heavy metal ions, the duration of the lethal mean time is different. The value of the coefficient of endurance under the influence of heavy metals on the horn extract decreases from high to low concentrations. At subthreshold concentrations, this coefficient cannot be established due to the absence of 100 % death of individuals until the end of the acute experiment. The values of the adaptation coefficient are the highest for highly toxic metal (Cu 2+ ) and the lowest for weakly toxic (Mn 2+ ). Under the action of copper ions, the adaptation of animals to the effects of the toxicant is temporary, followed by depression.

Arsenic is a well-known environmental toxicant and carcinogen, which has been epidemiologically proved related to the increased hepatic disorders. Researches have shown that aseptic inflammation and abnormal immune response are associated with arsenic-induced liver injury. However, the immunotoxic effects of liver have not been extensively characterized. Ginkgo biloba extract (GBE), a natural products of G. biloba leaves with proven anti-inflammatory and potential immunoregulatory activities, was used as intervention agent to explore its protective effects on arsenic-induced hepatotoxicity. Thus, the underlying mechanism of the immunotoxic effects on arsenic-induced liver injury were investigated in 2.5, 5.0, and 10.0 mg/kg NaAsO2 of Wistar rats for 16 weeks. Subsequently, GBE was used as intervention agent in 50 mg/kg for 6 weeks after cessation of arsenic exposure. The ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-β1, and IL-10 in serum and liver were detected. Meanwhile, the notable activation of aseptic inflammation-related molecule TLR4 and its downstream targets MyD88 and NF-κB in the liver were observed. In this work, we confirmed that subchronic exposed to arsenic triggered the infiltration of inflammatory cells in rat liver, coupled with obvious histopathological changes and aberrant hepatic serum biochemical parameters. Meanwhile, imbalanced immune response was verified by the notable abnormal ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-β1, and IL-10 in serum and liver of arsenic exposed rats. Further, the level of TLR4, MyD88, and NF-κB in liver both transcription and translation activity were raised. Subsequently, GBE markedly mitigated arsenic-induced liver injury, most impressively, post treatment with GBE prominently suppressed the overactivated inflammatory-related TLR4-MyD88-NF-κB pathway and evidently decreased the secretion of inflammation cytokines. Meanwhile, the disturbance of pro- and anti-inflammatory response was reversed. We concluded that the disruption of pro- and anti-inflammatory T-cells balance caused by cytokines mediated cell–cell interactions may be one of the mechanisms underlying arsenic-induced liver injury and that GBE intervention exerts an evidence protective effects, which might be closely associated with the suppression of inflammatory-related TLR4 pathway.

Problem. Cr (III) ions are dangerously toxic for the hydrobionts of water system of the Dnieper River basin. The ions have not been previously studied in relation to their effect on a number of pond snail species. Aim. Hence, the aim of this work is to determine the range of concentrations of Cr (III) in aquatic environment that cause each of the subsequent phases of pathological process in pond snails: poisoning by the aforementioned toxicant, and presence of the complexes of symptoms of the pathological or adaptive nature that are typical for each phase. Methods.The study was conducted in 2018 in the laboratory of zoology of invertebrates of Zhytomyr Ivan Franko State University on 344 individuals of pond snails of the species Lymnaea atra, L. callomphala and L. turricula. The toxicological experiment was performed according to the technique of V. A. Alekseyev, the rate of heartbeat by D. A. Vyskushenko, the rate of branchial respiration by V. I. Zhadin, the mean daily food intake by A. P. Sushkina, the trematode (Trematoda) infection rates and morphological examination by T. A. Ginetsinskaya. Main results. Cr (III) ions are water-soluble endogenic, highly poisonous toxicant, which locally affects the respiratory branchial epithelium and skin epithelium of pond snails. The depression, and later the termination of aerobic respiration lead to their death from asphyxia. The course of poisoning is five-phase. At 0.5 MPC Cr (III) all vital functions of pond snails are carried out at the normal level (indifference phase). At concentrations of 1-2 MPC, Cr (III) ions cause an increase in their heart rate, intensity of branchial respiration, nutrition and digestion, locomotion (muscle) activity (stimulation phase). At 3 MPC of Cr (III) ions, the depression phase of intoxication develops, with the complex of symptoms including bradycardia, a sharp weakening of respiratory and trophic functions and muscle activity, with increasing degrees of hydremia, pastosity, necrosis of the respiratory epithelium and underlying tissues, and the occurrence of bleeding and hemorrhage (depressive, sublethal and lethal phases). Conclusions. The studied species of pond snails are highly sensitive to the action of Cr (III) ions and can be suggested for use as test objects in the system of hydroecological monitoring of terrestrial waters of Ukraine.

Effects of cadmium chloride on the production of antioxidants such as reduced glutathione (GSH) inClarias gariepinusand how such effects can be ameliorated through administration of vitamins were investigated.C. gariepinusfingerlings were exposed to sub-lethal concentrations of Cd(00, 12mg/L, 16mg/L, 20mg/L and 24mg/L) with replicate in each case. 12mg/L each of the vitamins were administered across all bud. Fresh concentrations of both toxicant and vitamins were administered every 72 hours for a period of 12 weeks every time the water medium was changed. 3 samples of the fish were randomly selected and sacrificed from each aquarium tank every 2 weeks. The gills, kidneys and liver were excised from these specimens, homogenized in sodium phosphate buffer and then assayed for GSH production levels in each case. From the results: In Cd only group, the highest GSH level produced in the liver was 38.85±0.07µg/ml. In the liver of samples of CdVA group, the value (93.97±0.07µg/ml) increased then followed by the gill (67.72±0.13µg/ml). In CdVC, the GSH production level in the gill (39.76±0.07µg/ml) was relatively higher than livers and kidneys of the samples. In CdVE, the kidney produced the highest GSH value of 32.89±0.10µg/ml. The elicitation and utilization of the antioxidant at one point or the other were adopted by the fish in dealing with the effects of the toxicant especially in the presence of the vitamins. Higher concentrations of the vitamins could facilitate the understanding of the effects of the vitamins in mitigating the effects of the toxicant.

Mytilus edulis embryo-larval development is often used as a bioassay to evaluate the negative impact of contaminants and environmental conditions. The toxicity criteria used in most protocols is the proportions of normal and abnormal larvae. The variety of abnormalities were described and classified, but further development of abnormal larvae remains obscure. This study aimed to reveal the possibility of correction of the morphological abnormalities after short-term exposure (48 h) in a variety of K2Cr2O7 concentrations. For this purpose, abnormal larvae, which developed under the negative influence of the series of K2Cr2O7 concentrations were transferred into clean seawater and studied after further 24 and 48 h. The obtained data, concerning changes in larval morphology, growth and survival rates during washing show that the abnormal larvae have enough capability to recover the normal D-shell structure. Moreover, restoration of the D-shell is possible even after exposure with concentration of the toxicant higher than the average effective one. The present research also pointed out that the development of larval shell (even abnormal one) is positively correlated with ability of the larvae to reconstruct D-shell and their survival rate. High mortality during washing occurs only at toxicant concentrations when no shell was formed within 48 h. Thus, the existence of the shell after 48 h exposure in the toxicant could indicate reversibility of the negative impact and help to distinguish the delay in development from its arrest.

Introduction Studies suggest tobacco and cannabis co-users may experience greater toxicant exposure than exclusive cigarette (ET) smokers. No study has systematically tested differences in toxicant exposure among co-users, exclusive cannabis (ECa) smokers, and ET smokers. Aims and Methods Adult daily cigarette smokers and/or weekly cannabis smokers completed two laboratory visits. Co-users (n = 19) tested positive for urinary 11-nor-9-carboxy-Δ 9-tetrahydrocannabinol (THCCOOH), self-reported cannabis use ≥1 per week, and smoked ≥5 cigarettes per day (CPD). ET smokers (n = 18) denied past month cannabis use, tested negative for urinary THCCOOH and smoked ≥5 CPD. ECa smokers (n = 16) tested positive for urinary THCCOOH, self-reported cannabis use ≥1 per week, and denied past month tobacco use (NicAlert Results Co-users and ET smokers had higher levels of exhaled carbon monoxide, total nicotine equivalents, metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNAL), and all four measured mercapturic acids (measures of volatile organic compounds) than ECa smokers (ps < .005). ET smokers (geometric mean = 7220.2 pmol/mg) had higher levels of 2-hydroxypropylmercapturic acid than co-users (geometric mean = 5348.7 adjusted p = .009). Phenanthrene tetraol did not differ by group (p > .05). Conclusions Co-users and ET smokers demonstrated comparable levels of biomarkers of exposure to harmful constituents despite smoking similar amounts of tobacco. ECa smokers demonstrated lower levels of toxicant exposure for most biomarkers. Implications Although ECa smokers are exposed to significantly lower levels of harmful constituents compared with co-users and exclusive cigarette smokers, this group is still exposed to higher levels of toxicants than observed in studies of nonsmokers. Additionally, these three groups were exposed to similar levels of phenanthrene tetraol. It is important to account for cannabis use in studies examining biomarkers of exposure among cigarette smokers. Additionally, further research is needed examining exposure to harmful chemicals among various types of cannabis and tobacco users.

Microorganisms are known for their ability to adapt easily to any environment, forming specific ecosystems capable of surviving in harsh media. White phosphorus is one of the most dangerous and toxic pollutants, whose widespread use for various industrial and military purposes creates conditions for environmental pollution. It has previously been shown that some microbial cultures can adapt to the presence of white phosphorus in the environment, oxidizing it to a phosphate and then using it as a source of biogenic macronutrients. In prior studies, we have demonstrated the possibility of white phosphorus biodegradation by the fungal strains of Aspergillus niger. However, it is important to study the resistance of this species to such a toxic substance as white phosphorus. There may be several probable mechanisms, including the following: the cell wall of the fungus is a barrier to the penetration of white phosphorus into the cell, in which case an increase in the thickness of the cell wall should be observed in response to the impact of the toxicant; a mechanism associated with the expression of stress genes and the production of proteins involved in the disposal of toxins, including white phosphorus. In addition, white phosphorus causes an overall activation of metabolism, accompanied by an increase in the number and size of mitochondria in the cells. It is likely that the active forms of oxygen produced by mitochondria are involved in the detoxification of both white phosphorus and its transformation products. Microscopic and proteomic studies have confirmed the presence of the above-mentioned resistance mechanisms.

Dimethachlor is a synthetic herbicide, belonging to the chloroacetanilide group, that inhibits the undesirable growth of weeds via the suppression of very longchain fatty acid synthesis. Although dimethachlor has been shown to run off from agricultural fields into aquatic ecosystems, the toxicity of dimethachlor on aquatic invertebrates and vertebrates is unknown. In our study, we assessed the toxicity of dimethachlor on developing zebrafish embryos by analyzing viability, hatching ability, and phenotypic changes. Embryonic viability decreased from 48 h post-fertilization (hpf) at the highest concentration of dimethachlor. Decreased hatching ratio, shortened body length, and pathological changes in the eye, heart, and yolk sac were observed at sub-lethal concentrations. Additionally, dimethachlor increased the number of apoptotic cells and level of reactive oxygen species 120 hpf. Our results indicate that dimethachlor may act as an anti-developmental toxicant when accumulated in an aquatic environment.Dimethachlor is a synthetic herbicide, belonging to the chloroacetanilide group, that inhibits the undesirable growth of weeds via the suppression of very longchain fatty acid synthesis. Although dimethachlor has been shown to run off from agricultural fields into aquatic ecosystems, the toxicity of dimethachlor on aquatic invertebrates and vertebrates is unknown. In our study, we assessed the toxicity of dimethachlor on developing zebrafish embryos by analyzing viability, hatching ability, and phenotypic changes. Embryonic viability decreased from 48 h post-fertilization (hpf) at the highest concentration of dimethachlor. Decreased hatching ratio, shortened body length, and pathological changes in the eye, heart, and yolk sac were observed at sub-lethal concentrations. Additionally, dimethachlor increased the number of apoptotic cells and level of reactive oxygen species 120 hpf. Our results indicate that dimethachlor may act as an anti-developmental toxicant when accumulated in an aquatic environment.

Toxicant resistance is a complex trait, affected both by genetics and the environment. Like most complex traits, it can exhibit sexual dimorphism, yet sex is often overlooked as a factor in studies of toxicant resistance. Paraquat, one such toxicant, is a commonly used herbicide and is known to produce mitochondrial oxidative stress, decrease dopaminergic neurons and dopamine (DA) levels, and decrease motor ability. While the main effects of paraquat are well-characterized, less is known about the naturally occurring variation in paraquat susceptibility. The purpose of this study was to map the genes contributing to low-dose paraquat susceptibility in Drosophila melanogaster, and to determine if susceptibility differs between the sexes. One hundred of the Drosophila Genetic Reference Panel (DGRP) lines were scored for susceptibility via climbing ability and used in a genome-wide association study (GWAS). Variation in seventeen genes in females and thirty-five genes in males associated with paraquat susceptibility. Only two candidate genes overlapped between the sexes despite a significant positive correlation between male and female susceptibilities. Many associated polymorphisms had significant interactions with sex, with most having conditionally neutral effects. Conditional neutrality between the sexes probably stems from sex-biased expression which may result from partial resolution of sexual conflict. Candidate genes were verified with RNAi knockdowns, gene expression analyses, and DA quantification. Several of these genes are novel associations with paraquat susceptibility. This research highlights the importance of assessing both sexes when studying toxicant susceptibility.

Common carp (Cyprinus carpio) is one of the most important cultured fish species in Poland. The aims of our study were to determine the concentration of essential minerals in the muscle tissue of carp obtained from a pond culture and to compare the content of these minerals with the physiological norms of nutrition for the Polish population, Recommended Dietary Allowances (RDA), and Estimated Average Requirements (EAR). The non-carcinogenic and carcinogenic risk by assessment of the Estimated target hazard quotients (THQ), total target hazard quotients (ΣTHQ), and carcinogenic risk were also studied. The muscle tissue of the carp was rich in macroelements. The pattern significance gradation of element concentrations was as follows: Na > K > Ca > P > Mg > Al > Zn > Fe > Cu > Mn > Cr > Se > Co. The concentration of toxic heavy metals in the samples was lower than the maximum allowable level of metals in food products. The risk of consumption of toxicants by an adult at a daily intake of 100 g of fish was 1.45% for Pb, 0.1% for Hg, 0.02% for Cd, and 0.02% for As, compared to the allowable daily intake for each toxicant. The value of the target hazard quotients of each metal was less than 1, indicating that the intake of a single metal through the consumption of carp meat does not pose a considerable health hazard. The total value of the target hazard quotients was also less than 1, indicating the safety of the combined effects of the chemicals. The major risk contributor was Pb with 82.9%, followed by Hg (9.38%), As (6.43%), and Cd (1.29%).

In insects, the cytochrome P450 CYP6B family plays key roles in the detoxification of toxic plant substances. However, the function of CYP6 family genes in degrading plant toxicants in Tribolium castaneum, an extremely destructive global storage pest, have yet to be elucidated. In this study, a T. castaneum CYP gene, TcCYP6BQ7, was characterized. TcCYP6BQ7 expression was significantly induced after exposure to essential oil of the plant Artemisia vulgaris (EOAV). Spatiotemporal expression profiling revealed that TcCYP6BQ7 expression was higher in larval and adult stages of T. castaneum than in other developmental stages, and that TcCYP6BQ7 was predominantly expressed in the brain and hemolymph from the late larval stage. TcCYP6BQ7 silencing by RNA interference increased larvae mortality in response to EOAV from 49.67% to 71.67%, suggesting that this gene is associated with plant toxicant detoxification. Combined results from this study indicate that the CYP6 family gene TcCYP6BQ7 likely plays a pivotal role in influencing the susceptibility of T. castaneum to plant toxicants. These findings may have implications for the development of novel therapeutics to control this agriculturally important pest.

Toxicology supports health risk assessments that generate exposure limits for chemicals. A toxic effect is presumed proportional to the concentration of the proximal toxicant at the target site of action. Uptake, distribution, metabolism and excretion of a toxicant explain the action of the agent and the variation in potency between exposure circumstances, species, and agents with similar mode of action. The proximal toxicant may be the parent compound or a product of metabolism of the toxic agent. Portals for entry into the body in the occupational environment are primarily inhalation and skin absorption. The most prominent determinants of absorption are physical state, particle size and lipid solubility. The liver is the most prominent organ for metabolism of toxicants, oxidation by Cytochrome P450 enzymes the most prominent metabolic pathway for activation and detoxification. Excretion pathways include exhalation of volatile compounds, transport of polar compounds to urine by the kidney and transport of lipid soluble compounds to feces via bile. Examples of agents and detailed discussion of the structure of organ systems are given. Keywords: Cytochrome P450; uptake; distribution; xenobiotics; exposure limits

Aconitine (AC) is well-known as the main toxic ingredient and active compound of Aconitum species, of which several aconites are essential herbal medicines of Traditional Chinese Medicine (TCM) and widely applied to treat diverse diseases for their excellent anti-inflammatory, analgesic, and cardiotonic effects. However, the cardiotoxicity and neurotoxicity of AC attracted a lot of attention and made it a favorite botanic poison in history. Nowadays, the narrow therapeutic window of AC limits the clinical application of AC-containing herbal medicines; overdosing on AC always induces ventricular tachyarrhythmia and heart arrest, both of which are potentially lethal. But the underlying cardiotoxic mechanisms remained chaos. Recently, beyond its cardiotoxic effects, emerging evidence shows that low doses of AC or its metabolites could generate cardioprotective effects and are necessary to aconite's clinical efficacy. Consistent with TCM's theory that even toxic substances are powerful medicines, AC thus could not be simply identified as a toxicant or a drug. To prevent cardiotoxicity while digging the unique value of AC in cardiac pharmacology, there exists a huge urge to better know the characteristic of AC being a cardiotoxic agent or a potential heart drug. Here, this article reviews the advances of AC metabolism and focuses on the latest mechanistic findings of cardiac efficacy and toxicity of this aconite alkaloid or its metabolites. We also discuss how to prevent AC-related cardiotoxicity, as well as the issues before the development of AC-based medicines that should be solved, to provide new insight into the paradoxical nature of this ancient poison.

Oocyte mitochondria are unique organelles that establish a founder population in primordial germ cells (PGCs). As the oocyte matures in the postnatal mammalian ovary during folliculogenesis it increases exponentially in volume, and the oocyte mitochondria population proliferates to about 100 000 mitochondria per healthy, mature murine oocyte. The health of the mature oocyte and subsequent embryo is highly dependent on the oocyte mitochondria. Mitochondria are especially sensitive to toxic insults, as they are a major source of reactive oxygen species (ROS), they contain their own DNA (mtDNA) that is unprotected by histone proteins, they contain the electron transport chain that uses electron donors, including oxygen, to generate ATP, and they are important sensors for overall cellular stress. Here we review the effects that toxic insults including chemotherapeutics, toxic metals, plasticizers, pesticides, polycyclic aromatic hydrocarbons (PAHs), and ionizing radiation can have on oocyte mitochondria. This is very clearly a burgeoning field, as our understanding of oocyte mitochondria and metabolism is still relatively new, and we contend much more research is needed to understand the detrimental impacts of exposure to toxicants on oocyte mitochondria. Developing this field further can benefit our understanding of assisted reproductive technologies and the developmental origins of health and disease (DOHaD).Summary sentence Oocyte mitochondria are unique organelles, which are sensitive targets to various toxicants.

Di-(2-ethylhexyl) phthalate (DEHP) is a male reproductive toxicant. This research is aimed at investigating the effect of pubertal DEHP exposure on testicular endoplasmic reticulum (ER) stress and germ cell apoptosis. Five-week-old male mice were orally administered with DEHP (0, 0.5, 50, or 500 mg/kg/day) for 35 days. Testis weight and sperm count were reduced in mice exposed to 500 mg/kg/day DEHP. The number of seminiferous tubules in stages VII-VIII, mature seminiferous tubules, was reduced and the number of seminiferous tubules in stages IX-XII, immature seminiferous tubules, was elevated in mice treated with 500 mg/kg/day DEHP. Numerous apoptotic germ cells were observed in mouse seminiferous tubules exposed to 50 and 500 mg/kg/day DEHP. Moreover, cleaved caspase-3 was elevated in mouse testes exposed to 500 mg/kg/day DEHP. In addition, Bcl-2 was reduced and Bax/Bcl-2 was elevated in mouse testes exposed to 500 mg/kg/day DEHP. Additional experiment showed that GRP78, an ER molecular chaperone, was downregulated in mouse testes exposed to 500 mg/kg/day DEHP. Testicular p-IRE-1α, p-JNK, and CHOP, three markers of ER stress, were upregulated in mice exposed to 500 mg/kg/day DEHP. These results suggest that pubertal exposure to high doses of DEHP induces germ cell apoptosis partially through initiating ER stress in testes.

Profenofos is an endocrine-disrupting chemical that can enter into the aquatic ecosystem either through surface runoff or through percolation of a toxicant from the soil. In order to clarify the effect of profenofos on the developmental stages of zebrafish, the embryos were treated with serial dilutions of profenofos (0%, 10%, 25%, and 50% of LC50). Embryos were treated with profenofos for 7 days or until hatching. The toxic endpoints assessed include hatching time, survival, malformation, and heartbeats of the embryos. In a 96-h test on zebrafish embryos, the LC50 of profenofos was 0.057 mg/L. Profenofos considerably lowered survival, increased abnormalities at different ontogenetic stages, and developed malformations of different organs in a concentration-dependent fashion. The identified developmental malformations were fluid accumulation, impaired jaw, short tail, ruptured pectoral and caudal fin, curved body, thin yolk sac tube, and deformed heart. The way of looping arrangement of the heart at the early stage of embryos was significantly influenced by the higher concentration of profenofos. Heartbeat is also reduced significantly in a concentration-dependent fashion. The results show that the zebrafish are susceptible to profenofos even at lower concentrations in the initial stage. Therefore, when used in agricultural areas adjacent to the aquatic environment, endocrine-disrupting chemicals should be used in an appropriate manner.

The aim of this study was to investigate the expression of metallothionein genes in the liver and kidneys of rats with acute cadmium poisoning.Simulation of poisoning with cadmium chloride was carried out on white outbred female rats, divided into 4 groups depending on the dose of the injected toxicant. RNA samples isolated from rat liver and kidneys were used as research materials.The multiplicity of expression of the MT3 gene in the kidneys increased at the lowest dose of CdCl2 , which was used in this experiment (0.029 mg / kg); with increasing dosage, the expression level decreased, but not lower than the control values. Analysis of the expression of the same gene in the liver showed a tendency towards a decrease in the content of transcripts with increasing dose. The frequency of expression of the MT2A gene at higher doses of CdCl2 increased both in the liver and in the kidneys.In the present work, statistically significant dose-dependent changes in the expression multiplicity of metallothionein genes were detected 24 hours after CdCl2 administration. The revealed differences in the level of transcriptional activity of metallothionein genes require further investigation, since there are probably differences in the level of gene expression at earlier and later periods of toxicant action.

Graphical abstract, Highlights • Aroclor1260 worsened diet-induced steatohepatitis in CAR and PXR knockout mice. • CAR and PXR ablation increased gut microbiome diversity and modified composition. • Improved bacterial diversity did not protect mice from PCB-mediated toxicity. • Toxicant-nuclear receptor interactions modulate the gut-liver axis., Polychlorinated biphenyls (PCBs) are persistent organic pollutants associated with non-alcoholic fatty liver disease (NAFLD). Previously, we demonstrated that the PCB mixture, Aroclor1260, exacerbated NAFLD, reflective of toxicant-associated steatohepatitis, in diet-induced obese mice, in part through pregnane-xenobiotic receptor (PXR) and constitutive androstane receptor (CAR) activation. Recent studies have also reported PCB-induced changes in the gut microbiome that consequently impact NAFLD. Therefore, the objective of this study is to examine PCB effects on the gut-liver axis and characterize the role of CAR and PXR in microbiome alterations. C57Bl/6 (wildtype, WT), CAR and PXR knockout mice were fed a high fat diet and exposed to Aroclor1260 (20 mg/kg, oral gavage, 12 weeks). Metagenomics analysis of cecal samples revealed that CAR and/or PXR ablation increased bacterial alpha diversity regardless of exposure status. CAR and PXR ablation also increased bacterial composition (beta diversity) versus WT; Aroclor1260 altered beta diversity only in WT and CAR knockouts. Distinct changes in bacterial abundance at different taxonomic levels were observed between WT and knockout groups; however Aroclor1260 had modest effects on bacterial abundance within each genotype. Notably, both knockout groups displayed increased Actinobacteria and Verrucomicrobia abundance. In spite of improved bacterial diversity, the knockout groups however failed to show protection from PCB-induced hepato- and intestinal- toxicity including decreased mRNA levels of ileal permeability markers (occludin, claudin3). In summary, CAR and PXR ablation significantly altered gut microbiome in diet-induced obesity while Aroclor1260 compromised intestinal integrity in knockout mice, implicating interactions between PCBs and CAR, PXR on the gut-liver axis.

Metals cause popular attention worldwide due to their non-degradability and universal distribution in the aquatic ecosystem. In this study, the single, binary, and ternary combined toxicity of copper, cadmium, and lead toward survival rate of Daphnia magna were investigated based on different level fixed equivalenteffect concentration ratios. Furthermore, the combined toxicity was predicted by concentration addition and independent action models based on an established concentration-response relationship of a single toxicant and compared with the experimental data. The results indicated both binary and ternary mixture of the three metals had a strongly synergistic effect (EC50mix

Maternal toxicant exposure during gestation can have deleterious effects on neurobehavioral development of the offspring. The potential risks engendered by paternal toxicant exposure prior to conception have been largely understudied. Recently, we found that chronic THC exposure prior to conception in male rats causes long-lasting behavioral impairment in their offspring. The current study examined the effects of chronic preconception exposure to cannabis smoke extract in Sprague-Dawley rats at two different phases in sperm development. One group received daily subcutaneous (sc) injections of THC in cannabis extract at 4 mg/kg/day for 28 days until three days prior to mating with untreated females (late exposure group). Another group received the same regimen except they underwent 56 days of drug abstinence prior to mating (early exposure group). These were compared with a control group treated with vehicle. The offspring underwent a battery of tests for behavioral function to assess motor, emotional and cognitive function. On the elevated plus maze test, the offspring of both paternal cannabis smoke extract (CSE) exposure groups had significantly more time on the open arms than control offspring, indicative of greater risk-taking behavior. No significant main effects of CSE exposure were seen on adolescent or adult locomotor activity in the figure-8 apparatus. In the novel object recognition test, there was a significantly greater drop-off in novel object preference across the session in the male, but not female offspring of the late exposure group. There was also a sex-selective effect of paternal CSE treatment in the 16-arm radial maze test of memory function. Female offspring of the late exposure group had significantly more working memory errors than control females in the first half of the 12-session training sequence. No significant effects were seen in the operant visual signal sustained detection test of attention. This study shows that there are long-lasting behavioral consequences of preconception CSE exposure through the paternal lineage in rats.

Crude oil toxicity possess a major threat to the aquatic ecosystem in the Niger Delta. This study investigated the inherent tolerability potential of hydrocarbon degrading strain of Citrobacter amalonaticus - Y2ESWS1 to crude oil toxicity. Sediment samples were obtained from selected locations and subjected to bacteriological analysis using standard methods. Bacterial identification result revealed taxonomic group of hydrocarbon utilizing bacteria species including Citrobacter amalonaticus strain Y2ESWS1. Toxicity testing revealed that the toxicant concentration and exposure time were key variables that mediated toxicity. A second-order polynomial regression model revealed significant (P

Di-(2-ethylhexyl) phthalate is representative of Phthalate esters (PAEs), which is one of the most widely used plasticizer and known to act as a reproductive toxicant. However, little is known about the toxicity and pathological process of DEHP exposure in male reproductive system in terms of different concentrations and time points. In this study, peripubertal male Sprague Dawley rats were continually exposed to different DEHP doses (100 mg/kg, 500 mg/kg, and 900 mg/kg) and periods (7 days, 14 days, 21 days, 28 days, and 35 days) during critical periods for sexual maturity. The reproductive parameters have been investigated, including testicular morphology, serum testosterone level, and testicular P450scc, 3β-HSD, and PCYP17 levels. We observed disarrangement of testicular spermatogenic epithelium coupled with decrease of serum testosterone, testicular P450scc, 3β-HSD, and PCYP17 levels, and these changes were more obvious with increase of both the exposure time and dosage. Then trend of the time-dose response to DEHP exposure and the pathological process in germ cells were estimated. The results of this study suggested that DEHP exposure could affect the male reproductive system and the degree of adverse effect depended on the dose and extent of exposure.

Current standardized laboratory test protocols use model species that have limitations to accurately assess native species responses to stressors. We developed and tested a novel acute insitu protocol for testing field-collected organisms. We used Asellus aquaticus and NaCl as a reference toxicant to test for the effects of location (laboratory vs. insitu), medium (synthetic vs. field water), substrate (presence vs. absence), and protocol replicability. We further tested the protocol using groundwater-adapted isopods: Proasellus assaforensis for the effect of location, P. cavaticus of medium and P.lusitanicus of substrate. Our results showed that A.aquaticus’ lethality obtained with the novel acute insitu protocol did not significantly differ from those from laboratory testing. However, laboratory tested P.assaforensis showed a higher sensitivity, suggesting that its acclimation to laboratory conditions might have pernicious effects. A. aquaticus and P. cavaticus showed a higher mortality using synthetic medium insitu and under laboratory conditions, which overestimated the stressor’s effect. Besides, substrate use had no significant effect. The novel acute insitu protocol allows the use of native species under realistic scenarios. It is particularly well adapted for assessing the risk of groundwater ecosystems but it can be applied to a wide range of ecosystems.

Effects of MPC, 2 MPC, and 3MPC water solutions of potassium nitrate and biotic factors (trematode infection and “gill pregnancy”) were studied on the duration of locomotion and beat frequency of epithelial cilia of outer demibranchs of Sinanodonta woodiаna (Lea, 1834). The species has recently invaded the system of water bodies of Ukraine. It has occupied numerous water bodies in the Kiliya distributary of Danube Delta, establishing populations of density and biomass. Statistically significant differences by the studied parameters of ciliary epithelium (duration of locomotion and beat frequency of cilia) were not observed in the control group of non-infected males and latent females of S. woodiana. In females with “gill pregnancy”, the duration of ciliary locomotion decreased by 1.5 times, and beat frequency by 1.4 times (P>99.9 %). It should be noted that the outer surface of demibranchs of female mollusks was completely covered by the filled to the brim marsupial pockets. Thus, the functional load of gills is high, leading to the development of compensatory processes in experimental animals. The processes induce increased effectiveness of protective factors that counteract them. Another biotic factor negatively affecting the experimental pond mussels was the high rates of trematode infection in the hosts’ reproductive glands which contained sporocysts and cercariae of Rhipidocotyle campanula Dujardin, 1845. Prevalence of that infection ranged from 50 to 100 %. These rates of infection were associated with sharply declining functions of cilia of the gill epithelium in studied animals. The compound pathogenic influence of parasite and “gill pregnancy” factors even more affected the functional parameters of outer gill ciliary epithelium. The MPC levels of toxicant in the water medium were accompanied with the first symptom of intoxication of the Chinese pond mussel, the stage of stimulation. At that point, the functional parameters of epithelial cilia of “pregnant” females and in moderately and weakly infected mollusks of both sexes increased in response to exposure to the toxic factor. With the growing concentrations of toxicant to 2 MPC and 3 MPC, the experimental pond mussels developed the pathological process of intoxication, which progressed from the stage of depression to sublethal and lethal stages. Accordingly, the locomotion activity of ciliary epithelium increasingly declined and, in the end, stopped. The “gill pregnancy” and high rates of trematode infection exacerbated the consequences of the process.

The general toxicity assays for evaluating the risk of aquatic environment were commonly based on single-species test organism models. Thus, the lack and conflict of the different responses among species had hindered researchers to assess the real toxicity of a target toxicant. Therefore, the difference between the test species and their corresponding methodologies was investigated in this work and three species, Escherichia coli, Saccharomyces cerevisiae and Misgurnus anguillicaudatus (a fish), were chosen as the test organism for typical prokaryotes, eukaryotes, and vertebrates, respectively. More specifically, we investigated (i) the individual and combined toxicity of Cu2+ and Zn2+ by the three test organisms; (ii) the different evaluation manners for the test organisms, including IC50 and toxic unit (TU) model for microorganisms by respiratory toxicity assay and enzyme-substrate assay, while survival time for fish; and (iii) the states of test organism, including suspended and immobilized states for microorganisms. The combined effects, including synergistic (Vt Vp) and additive effects for the three species, were complex as that they were usually dose-dependent and could be changed by the different evaluation manners. The present work was useful for enriching of the associated theory and the insights from this work could open the way for further practical risk assessments.

Histopathological manifestation of castor bean seed as fish toxicant upon gastro-intestinal system of Tilapia (Oreochromis mossambicus) was investigated parallel with mohua oil cake as haemotoxic piscicidal agent in outdoor experimental tanks. Castor seed bean was proved to be an effective piscicide with activity potential comparative with mohua oil cake though the mortality rate was higher and quicker in the later. As plant derived toxicant castor bean exhibited strong histopathological lessions in intestinal mucosa and liver whereas, mohua oil cake exhibited severe respiratory distress to the test fish. Significant reduction of dissolved oxygen and concurrent increase in BOD1 of water under both the piscicides aggravated the distress of the test fish.

Purpose of review The purpose of this review is to describe epidemiologic and toxicological literature investigating how endocrine-disrupting chemicals (EDCs) affect mammary gland development and function, thereby impacting lactation duration. Recent findings Perfluoroalkyl and polyfluoroalkyl substances appear to reduce breastfeeding duration through impaired mammary gland development, lactogenesis, and suppressed endocrine signaling. Halogenated aromatic hydrocarbons have differing associations with lactation duration, likely because of the variety of signaling pathways that they affect, pointing to the importance of complex mixtures in epidemiologic studies. Although epidemiologic literature suggests that pesticides and fungicides decrease or have no effect on lactation duration, toxicology literature suggests enhanced mammary gland development through estrogenic and/or antiandrogenic pathways. Toxicological studies suggest that phthalates may affect mammary gland development via estrogenic pathways but no association with lactation duration has been observed. Bisphenol A was associated with decreased duration of breastfeeding, likely through direct and indirect action on estrogenic pathways. Summary EDCs play a role in mammary gland development, function, and lactogenesis, which can affect breastfeeding duration. Further research should explore direct mechanisms of EDCs on lactation, the significance of toxicant mixtures, and transgenerational effects of EDCs on lactation.

Fenvalerate, a synthetic pyrethroid insecticide, is an environmental endocrine disruptor and neurodevelopmental toxicant. An early report found that pubertal exposure to high-dose fenvalerate impaired cognitive and behavioral development. Here, we aimed to further investigate the effect of pubertal exposure to low-dose fenvalerate on cognitive and behavioral development. Mice were orally administered with fenvalerate (0.2, 1.0 and 5.0 mg/kg) daily from postnatal day (PND) 28 to PND56. Learning and memory were assessed by Morris water maze. Anxiety-related activities were detected by open-field and elevated plus-maze. Increased anxiety activities were observed only in females exposed to fenvalerate. Spatial learning and memory were damaged only in females exposed to fenvalerate. Histopathology observed numerous scattered shrinking neurons and nuclear pyknosis in hippocampal CA1 region. Neuronal density was reduced in hippocampal CA1 region of fenvalerate-exposed mice. Mechanistically, hippocampal thyroid hormone receptor (TR)β1 was down-regulated in a dose-dependent manner in females. In addition, TRα1 was declined only in females exposed to 5.0 mg/kg fenvalerate. Taken together, these suggests that pubertal exposure to low-dose fenvalerate impairs cognitive and behavioral development in a gender-dependent manner. Hippocampal TR signaling may be, at least partially, involved in fenvalerate-induced impairment of cognitive and behavioral development.

In the present paper, we study two eco-epidemiological models. The first one consists of a prey and two competing predators with SI-disease in prey species spreading by contacts between susceptible prey and infected prey. This model assumes linear functional response. The second model is the modification of the first one when the effect of toxicant is taken into account. In this paper, we examine the dynamical behavior of non-survival and free equilibrium points of our proposed model.

The pathogenetic mechanism of reproductive diseases is oxidative stress, which is manifested by an increase in lipid peroxidation and a decrease in antioxidant potential. The aim of the study was to develop a method for the correction of biochemical changes in the body of boars with toxicant-induced reproductive dysfunctions using drugs based on nanobiomaterials, based on reducing lipoperoxidation, neutralization of toxic substances by antioxidant protection increasing of animals and endocrine activity stimulating of their gonads. The article presents the results of research on the effectiveness of the complex drug ‘Karafand+OV,Zn’, which contains carotenoids, phytoandrogens and nanomaterials — nanoparticles of gadolinium orthovanadate, activated by europium, and zinc carbonate. Experimental toxicant-induced reproductive dysfunctions were caused by feeding sodium nitrate at a dose of 0.3 g NO3–/kg body weight. The drug was administered in a dose of 15 ml per male, orally, once a day for 14 days. Blood samples for test were taken before and on the 20th day after drug administration. Conventional biochemical methods were used, as well as chemiluminometry and enzyme-linked immunosorbent assay. There was a positive effect of the developed drug on the hormonal state (testosterone concentration increased by 91.8% (20.6 ± 0.32 nmol/l, p < 0.001), the content of vitamin A increased 1.3 times (0.65 ± 0.02 μmol/l, p < 0.001) and zinc by 47.6% (24.8 ± 0.86 μmol/l, p < 0.001), the dynamics of lipoperoxidation processes (the concentration of malonic dialdehyde in the serum was reduced by 53.2% (0.394 ± 0.01 μmol/l, p < 0.001)) and the system of antioxidant protection of boars (increased activity of catalase and superoxide dismutase in serum by 71.5% (41.4 ± 1.03 μmol/H2O2/l-min, p < 0.001) and 54.8% (8.98 ± 0.09 st. un./mgHb, p < 0.001), respectively), increased the content of reduced glutathione by 23.2%, indicators of the oxygen metabolism system (concentration 2,3-diphosphoglycerate increased 1.3 times (1.4 ± 0.03 mmol/l, p < 0.001), the activation of which reduces the hypoxic state. The total antioxidant activity of boars increased, as evidenced by a decrease in the light sum of chemiluminescence of serum by 47.6% (4.4 ± 0.15 un., p < 0.001). The results of research convincingly testify to the high efficiency of the use of the complex drug ‘Karafand+OV,Zn’ as a means of correction of toxicant-induced reproductive dysfunctions in boars and proves the possibility of its use in practical veterinary andrology

Xenobiotics have been documented to play crucial role in pathogenesis of human diseases. Phenyl hydrazine administration has been associated with hematotoxicity by altering iron metabolism and activating immune response. Telfaria occidentalis is a medicinal plant rich in phytochemicals and minerals that are immune boosters. This study investigated the effect of ethanol leaf extract of T. occidentalis against phenyl hydrazine induced anaemia and associated toxicities in rats. Phenyl hydrazine was exposed to rats through oral administration and ethanol leaf extract of T. occidentalis or vitamin E was administered to ameliorate the toxic effect of the toxicant. This was followed by evaluation of haematological parameters, body weight, and serum protein biomarkers like bilirubin, albumin, total bilirubin. Phenyl hydrazine induced anaemia with significant reduction of blood components like haemoglobin, erythrocytes, leukocytes with concomitant reduction in the body weight of the rat compared to the control. Phenyl hydrazine also compromised serum protein homeostasis as evidenced by elevated serum total protein, albumin, bilirubin and globulin levels. Nevertheless, treatment with ethanol leaf extract of T. occidentalis modulates all the anomalies suggesting its ameliorating effects against phenyl hydrazine-induced anaemia, and may be useful in the treatment/management of chemically induced anaemia or other related diseases.

Cadmium (Cd) is a toxic heavy metal with no known biological functions in the human body. Due to a considerably long biological half-life and very low rate of excretion, accumulation of Cd in different body organs (eg, liver, kidney, and testes) over time is associated with perturbed functioning of these organs. Recent studies have shown the extreme sensitivity of the testes to Cd toxicity. In testes, Cd has been reported to induce oxidative stress, apoptosis of spermatogenic cells, reduction in androgen production and sperm functions. Moreover, Cd in combination with other environmental toxicants may be responsible for the declining fertility of males in both animals and humans. Pinpointing how Cd toxicity affects various testicular processes will be imperative for the development of preventative measures to promote fertility among males. Therefore, in the present review, we summarize the recent findings related to the Cd-induced oxidative toxicity, apoptotic toxicity, steroidogenic toxicity, and spermatotoxicity, along with their possible mechanisms in testicular tissue of different animal species. In addition, the utilization of various antioxidant compounds, medicinal plants and other compounds for the management of Cd toxicity in testes is discussed.

Different environmental toxins especially heavy metals exist in soil, water, and air recording toxic effect on human, animal, and plant. These toxicant elements are widespread in environment causing various disturbances in biological systems. Numerous strategies have been applied recently to alleviate heavy metal contamination; however, most of these strategies were costly and seemed unfriendly to our environment. Probiotics are living cell bacteria with beneficial characteristics for human health. Lactobacillus and Bifidobacterium are the major probiotic groups; however, Pediococcus, Lactococcus, Bacillus, and yeasts are recorded as probiotic. The vital role of the probiotics on maintenance of body health was previously investigated. Probiotics were previously recorded to its powerful capacity to bind numerous targets and eliminate them with feces. These targets may be aluminum, cadmium, lead, or arsenic. The current review discusses the history of probiotics, detoxification role of probiotics caused by heavy metals, and mechanism of their action that modulate different signaling pathway disturbance associated with heavy metal accumulation in biological system.

The effects of sub-lethal concentrations of Corexit 9500 on growth and condition factor of juveniles of Clarias gariepinus was investigated after 21days, in 2018. 160 fishes were used as test organisms with a loading of 10/treatment and were exposed to 0.00, 0.0125, 0.025 and 0.05 ml/L concentrations of Corexit 9500. Treatments were in triplicate and Complete Randomised Design was adopted. The growth in length and weight of C. gariepinus was significantly higher in the control than the test treatments (P0.05); however, the DO of control was significantly higher (P < 0.05) than that of the treatments, with the lowest DO in the 0.05ml/l treatment. pH was acidic for all treatments including the control but was more acidic with increasing concentration of Corexit 9500. The pH value for each treatment was significantly different (P

Environmental health studies relate how exposures (eg, chemicals) affect human health and disease; however, in most cases, the molecular and biological mechanisms connecting an exposure with a disease remain unknown. To help fill in these knowledge gaps, we sought to leverage content from the public Comparative Toxicogenomics Database (CTD) to identify potential intermediary steps. In a proof-of-concept study, we systematically compute the genes, molecular mechanisms, and biological events for the environmental health association linking air pollution toxicants with 2 cardiovascular diseases (myocardial infarction and hypertension) as a test case. Our approach integrates 5 types of curated interactions in CTD to build sets of “CGPD-tetramers,” computationally constructed information blocks relating a Chemical- Gene interaction with a Phenotype and Disease. This bioinformatics strategy generates 653 CGPD-tetramers for air pollution-associated myocardial infarction (involving 5 pollutants, 58 genes, and 117 phenotypes) and 701 CGPD-tetramers for air pollution-associated hypertension (involving 3 pollutants, 96 genes, and 142 phenotypes). Collectively, we identify 19 genes and 96 phenotypes shared between these 2 air pollutant-induced outcomes, and suggest important roles for oxidative stress, inflammation, immune responses, cell death, and circulatory system processes. Moreover, CGPD-tetramers can be assembled into extensive chemical-induced disease pathways involving multiple gene products and sequential biological events, and many of these computed intermediary steps are validated in the literature. Our method does not require a priori knowledge of the toxicant, interacting gene, or biological system, and can be used to analyze any environmental chemical-induced disease curated within the public CTD framework. This bioinformatics strategy links and interrelates chemicals, genes, phenotypes, and diseases to fill in knowledge gaps for environmental health studies, as demonstrated for air pollution-associated cardiovascular disease, but can be adapted by researchers for any environmentally influenced disease-of-interest.

This research aims to understand ethical attitudes of the U.S. public towards the use of a toxicant to control wild pigs (Sus scrofa), a destructive invasive species whose population growth is prov...

Studies have shown that mammalian testes, in particular the Sertoli cells, are highly susceptible to exposure of environmental toxicants, such as cadmium, perfluorooctanesulfonate, phthalates, 2,5-hexanedione and bisphenol A. However, important studies conducted by reproductive toxicologists and/or biologists in the past have been treated as toxicology reports per se. Yet, many of these studies provided important mechanistic insights on the toxicant-induced testis injury and reproductive dysfunction, relevant to the biology of the testis and spermatogenesis. Furthermore, recent studies have shown that findings obtained from toxicant models are exceedingly helpful tools to unravel the biology of testis function in particular spermatogenesis, including specific cellular events associated with spermatid transport to support spermiogenesis and spermiation. In this review, we critically evaluate some recent data, focusing primarily on the molecular structure and role of microtubules in cellular function, illustrating the importance of toxicant models to unravel the biology of microtubule cytoskeleton in supporting spermatogenesis, well beyond information on toxicology. These findings have opened up some potential areas of research which should be carefully evaluated in the years to come.

Telomere integrity is critical for chromosomal stability. Evidence is rapidly growing that impaired telomere integrity may explain the higher risk of some diseases among specific occupations. This review aimed to assess the impact of occupational toxicants exposure on telomere length (TL) and to identify each toxicant's mechanism of action based on an integrative review of available evidence. A literature search was carried out using a set of keywords in different databases. Searches were limited to English publications from 2009 to 2019. Only studies that were using blood samples for TL measurements were included. Finally, 22 studies with a total of 5674 participants, were included. These studies included factory workers from various industries, farmers, coke-oven workers, hairdressers, traffic officers, and drivers. The toxicants were grouped into four categories, including persistent organic pollutants (7 articles), aromatic amines (9 articles), heavy metals (3 articles), and fine particulate matter (PM2.5) (3 articles). Different effects of the same toxicant in TL were observed in various occupations. Factors such as biological characteristics of exposed individuals (especially gene variations and age), diet, lifestyle, dose, and duration of exposure might have modulatory effects on mechanisms and extent of influences of toxicants on TL. Further possible modes of actions affecting the TL are oxidative stress, telomerase expression, systemic inflammation, epigenetic modification, and genotoxicity. In conclusion, various toxicants affect TL differently, but the effect may be moderated by improving the workers’ lifestyle. The involvement of different interrelated pathways may explain the differences in TL alterations.

There is a great need for novel in vitro methods to predict human developmental toxicity to comply with the 3R principles and to improve human safety. Human-induced pluripotent stem cells (hiPSC) are ideal for the development of such methods, because they are easy to retrieve by conversion of adult somatic cells and can differentiate into most cell types of the body. Advanced three-dimensional (3D) cultures of these cells, so-called embryoid bodies (EBs), moreover mimic the early developing embryo. We took advantage of this to develop a novel human toxicity assay to predict chemically induced developmental toxicity, which we termed the PluriBeat assay. We employed three different hiPSC lines from male and female donors and a robust microtiter plate-based method to produce EBs. We differentiated the cells into cardiomyocytes and introduced a scoring system for a quantitative readout of the assay—cardiomyocyte contractions in the EBs observed on day 7. Finally, we tested the three compounds thalidomide (2.3–36 µM), valproic acid (25–300 µM), and epoxiconazole (1.3–20 µM) on beating and size of the EBs. We were able to detect the human-specific teratogenicity of thalidomide and found the rodent toxicant epoxiconazole as more potent than thalidomide in our assay. We conclude that the PluriBeat assay is a novel method for predicting chemicals’ adverse effects on embryonic development. Electronic supplementary material The online version of this article (10.1007/s00204-020-02856-6) contains supplementary material, which is available to authorized users.