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Background: Carbon tetrachloride (CCl4) is a critical hepatotoxicant causing liver injury and fibrosis via hepatic production of reactive oxygen species (ROS). Apigenin (APG) is a natural bioactive compound and flavonoid antioxidant. We, therefore, evaluated whether APG could mitigate CCl4-mediated hepatotoxicity. Methods: Rats were randomly divided and administered APG and/or CCl4 in Control group, CCl4 group, APG + CCl4 groups (APG: 10 and 20 mg/kg bw) and APG groups (APG: 10 and 20 mg/kg bw) 2 times per week for 7 consecutive weeks. Result: Rats exposed to CCl4 demonstrated marked increases in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and monoamine oxidase (MAO) activities and decreased hepatic malondialdehyde (MDA) level compared to control. The hepatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) decreased appreciably. The CCl4 intoxication caused significant increases in inflammatory cytokines (IL-6 and TNF-α) and apoptosis markers, while the anti-inflammatory cytokines (IL-4 and IL-10) decreased with evident histopathological lesions compared to control. APG-dose-dependently-prevented these hepatic alterations.

Diabetes mellitus (DM) provokes reproductive impairments through endocrine disturbance, sperm deficits, and testicular oxidative inflammation. The study investigated the reproductive protective effects of resveratrol (RSV) against testicular oxidative inflammation, sperm/endocrine deficits, and insulin resistance in streptozotocin- (STZ-, 65 mg/kg) induced DM rat model. Male rats were randomly divided into 4 groups ( n = 6 ): control, DM, RSV (150 mg/kg bw, orally), and RSV+DM group (21 days). The nontreated DM rats showed marked decreases in serum insulin, reproductive hormones (T, LH, and FSH), and lipid profile levels compared to control. The homeostatic index of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were adversely modulated. Sperm count and motility were profoundly decreased, whereas sperm abnormality was significantly increased. The testicular activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA) level, along with inflammatory cytokines (TNF-α, IL-6, IL-4, and IL-10) were significantly dysregulated. The DM induced histopathological lesions compared to control rats. Interestingly, the RSV administration to DM rats attenuated the altered reproductive parameters, restored antioxidant mechanism, and anti-inflammatory responses with improved insulin resistance. RSV could prevent DM-induced reproductive deficits and insulin resistance via modulating oxidative stress-mediated testicular inflammation in rats.

Background: Betamethasone treatment is widely used and recommended worldwide. Although, there are no enough studies to look for the risk or potential alterations due to accumulation of this drug before fertilization. In addition, previous studies payed attention to intramuscular injection during pregnancy neglecting the long-term impact of the use of topical solutions. So, the aim of the present study was to determine this side effect. Methods: We used two doses of betamethasone: 0.02 and 0.2 mg/Kg b.w. were and at the end of the experimental period (after 3 weeks of delivery), six new-born rabbits of both sexes (1 new born rabbit per mother) were dissected under light anesthesia and heart samples were collected. All the measurements were performed in one assay. Result: The results of this study revealed maternal exposure to betamethasone prior to fertilization, induced oxidative stress, alterations in levels of enzymes. Furthermore, these biochemical alterations were supported by histopathological and ultrastructural observations. So, this study suggested that females; desiring to be pregnant, should stop treatment of psoriasis with betamethasone before fertilization to avoid heart toxicity of their offspring.

Background: Lead (Pb) is an environmental pollutant and has detrimental effects on human health. Apigenin (APG) is a flavonoid that have antioxidant, anti-inflammatory and antiallergic and cardioprotective so is used as treatment of many diseases. The aim of the present study was to evaluate the probable protective effect of APG against Pb-induced toxicity in rats. Methods: Adult male rats were given either Pb (as lead acetate; 20 mg/kg) alone or in combination with APG (20 mg/kg) daily for 4 weeks by intraperitoneally injection (i.p). At the end of the experimental period, Pb accumulation, lipid profile and testicular function alterations were assessed. In addition, histopathological changes in the testis were assessed. Result: Results revealed that Pb treatment significantly increased Pb concentrations in blood and testis of rats. Further, the blood levels of hormones related to testis were altered in Pb-treated rats. In parallel, low sperm count and sperm motility, increased sperm abnormalities and marked pathological changes in testis were observed. On the contrary, the treatment with both Pb and APG recorded amelioration of the deleterious effects of Pb, involving attenuation of changes in lipid profile and testicular hormonal levels, sperm parameters and pathological changes in Pb treated rat’s testis. In conclusion, it appears that dietary APG can ameliorate lead acetate induced hyperlipidemia and hypogonadism in male rats.

Background: Lead (Pb) is a heavy metal that represents an environmental toxicant causing serious health problem. Apigenin (APG) is a plant derived flavonoid with several therapeutic activities. So, the aim of the present study was to determine the protective effect of APG against Pb induced toxicity in cerebella of treated rats. Method: Twenty-four adult male rats (Rattus norvegicus) were used in the present study. They were divided into four groups of six animals per each one as follows: Group I: Rats were daily injected (i.p.) with normal saline as vehicle. Group II: Rats were daily injected (i.p) with lead acetate at a dose of 20 mg/kg b.w. Group III: Rats were daily injected (i.p) with lead acetate at a dose of 20 mg/kg (b.w.) followed by injection (i.p) with APG at dose of 20 mg/kg b.w. Group IV: Rats were daily injected (i.p) with APG at dose of 20 mg/kg b.w. At the end of the four-weeks experimental period, the animals were sacrificed and samples of blood and cerebellar tissue were collected. Results: Lead induced oxidative stress, alterations in levels of studied neurotransmitters, increase in the activities of acetylcholinesterase and increase in the level of the Il-6 and TNF-á and decrease in Il-4 and Il-10 and histological alterations in cerebellum. On the other hand, treatment with APG attenuates these alterations. suggesting that APG might play a neuroprotective role in lead induced neurotoxicity.

Background: Synthetic glucocorticoids, such as Betamethasone, are used for treatment of skin disease including Psoriasis. No enough evidences are present about the side effect of maternal exposure to betamethasone, before fertilization, on new-born. So, the goal of the present study was to determine these side effects on liver and kidney. Methods: In the present study, two doses of betamethasone (0.02 and 0.2 mg/kg b.w) were used. At the end of the experimental period (after 3 weeks of delivery), six new-born rabbits of both sexes (1 newborn rabbit per mother) were dissected under light anesthesia and blood, liver and kidney samples were collected. All the measurements were performed in one assay. Result: Maternal exposure to betamethasone, for 2 months before fertilization, induced toxicity in new-born rabbits and decrease the relative organ weight of liver and kidney in new-born rabbits. The biochemical changes involved induction of oxidative, alterations in hepatic and renal parameters. Moreover, structural changes in liver and kidney new-born rabbits were observed. So, this study suggested that females must take care in using treatment with betamethasone before fertilization to avoid toxicity of their offspring.

Background: Betamethasone is a synthetic glucocorticoid used for treatment of Psoriasis. Until now, the side effect of maternal exposure to topical betamethasone, prior to fertilization, on newborn is not clear. So, the aim of the present study was to determine this side effect. Methods: We used two doses of betamethasone: 0.02 and 0.2 mg/kg b.w. At the end of the experimental period (after 3 weeks of delivery), six new-born rabbits of both sexes (1 newborn rabbit per mother) were dissected under light anesthesia and blood and cerebellum samples were collected. All the measurements were performed in one assay. Result: The results of this study revealed that betamethasone can bioaccumulate in sera of rabbits treated mothers. Maternal exposure to betamethasone, for 2 months before fertilization, induced oxidative stress, alterations in levels of studied neurotransmitters and increase in activities of acetylcholinesterase and caspase-3 enzymes. Furthermore, these biochemical alterations were supported by histopathological observations. So, this study suggested that females; desiring to be pregnant, should stop treatment of psoriasis with betamethasone before fertilization to avoid cerebellar toxicity of their offspring.

The current study aims for the use of the solid-state technique as an efficient way for the preparation of zinc oxide nanoparticles (ZnONPs) as an antimicrobial agent with high concentration using sodium alginate as stabilizing agent. ZnONPs were prepared with three different concentrations: ZnONPs-1, ZnONPs-2, and ZnONPs-3 (attributed to the utilized different concentrations of zinc acetate, 1.5, 3 and 4.5 g, respectively). The as-fabricated ZnONPs (ZnONPs-1, ZnONPs-2, and ZnONPs-3) were used for the treatment of cellulosic fabrics as dressing materials for the diabetic wounds. DLS findings illustrated that the as-prepared ZnONPs exhibited average particle size equal to 78, 117, and 144 nm, respectively. The data also showed that all the formulated ZnONPs were formed with good stability (above −30 mv). The topographical images of cellulosic fabrics loaded with ZnONPs that were obtained by SEM confirmed the deposition of nanoparticles onto the surface of cellulosic fabrics with no noticeable agglomeration. The findings also outlined that the treated cellulosic fabrics dressings were proven to have enhanced bactericidal characteristics against the pathogenic microorganisms. The finding of wound contraction for the diabetic rats was measured after 21 days and reached 93.5% after treating the diabetic wound with cotton fabrics containing ZnONPs-2. Ultimately, the generated wound dressing (cellulosic fabrics loaded with ZnONPs) offers considerable promise for treating the wound infections and might be examined as a viable alternative to antibiotics and topical wound treatments.

This study aims to inspect the effects of Imidacloprid (IMI) acute toxicity in the ovaries of the red palm weevil (Rhynchophorus ferrugineus). The LC50 of IMI was determined to be 15.7 ppm. We assessed the biochemical changes resulting from treatment with four IMI concentrations (10, 15, 20 and 30 ppm). IMI reduced acetylcholine esterase activity in a dose-dependent manner. Glutathione (GSH) content decreased with increasing concentration of IMI; however, GSH was not affected and accompanied by an increase in catalase activity with the highest concentration of IMI. Lipid peroxidation increased steadily as IMI concentration increased. Based on the ultrastructural analyses of the follicle cells and the ooplasm of developing oocytes, acute IMI toxicity produced damaged yolk bodies, pale nuclei, and shrinking microvilli. Fractionation of rough endoplasmic reticulum, deformed mitochondria, and autophagic bodies were also observed. In conclusion, these ovarian pathobiochemical changes could be used as biomarkers of acute IMI exposure.

Background Acrylamide (ACR) is a well-proven neurotoxin and potential food carcinogen in humans and rodent models. Silymarin (SIL) is a flavonoid mixture isolated from seeds, leaves, and fruits of Silymarin marianum (milk thistle) that possesses a free-radical scavenging effect. Objective In this work, the primary focus was to investigate the efficacy of SIL to mitigate ACR-induced subacute neurotoxic effects and oxidative changes in rat cerebellum. Methods Adult male rats were treated intraperitoneally with ACR (50 mg/kg) with or without SIL (160 mg/kg). The neuropathology and biochemical parameters viz. lipid peroxidation (measured as levels of malondialdehyde or MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), serotonin (5-hydroxytryptamine; 5-HT), dopamine (DA), and cathepsin D (CTSD) in the cerebellum have been evaluated. Results The data showed that ACR induced redox disruptions as measured by increased MDA levels and inhibition of CAT, SOD, and GPx antioxidant enzyme activities. Besides, cerebellar monoamine neurotransmitters, 5-HT and DA, were depleted in ACR-treated rats. Furthermore, ACR administration caused a significant elevation of CTSD activity, indicating that ACR could trigger apoptosis or apoptosis-like death. At the tissue level, cerebellar cortex sections from ACR-treated animals were characterized by severe neuronal damage. The administration of SIL to ACR-treated rats remarkably alleviated all the aforementioned ACR-induced effects. Conclusion SIL has a potent therapeutic effect against ACR-induced cerebellar neurotoxicity in experimental rats via the attenuation of oxidative/antioxidative responses and the inhibition of CTSD-activity.

Methotrexate (MTX) is an efficient chemotherapeutic and immunosuppressant drug, but the hepatotoxicity of MTX limits its clinical use. Naringin (Nar) is a flavonoid derived from Citrus paradise, and has been shown to possess several pharmacological activities, including free-radical scavenging and antioxidant properties. In the present study, we first tested the possible protective effects of multiple doses of Nar against MTX-induced acute hepatotoxicity in rats, and then we investigated the growth inhibition and apoptotic effects of MTX and/or Nar against the HepG2 hepatocarcinoma cell line. Our in vivo results showed that Nar significantly reduced MTX-induced increases in serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and total bilirubin levels. Nar also reduced MTX-induced oxidative stress by significantly reducing liver malondialdehyde (MDA) and nitric oxide (NO) content and increasing superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH). In addition, Nar significantly counteracted MTX-induced increases in hepatic interleukin-6 and tumor necrosis factor-α (TNF-α). Further, Nar greatly protected hepatocyte ultrastructure against MTX-induced injury. In contrast, in vitro MTX and/or Nar treatment of HepG2 cells for 48 h exhibited a cytotoxic effect and induced apoptosis in a dose-dependent manner mediated by a significant increase in the Bax/Bcl-2 protein expression ratio. Noticeably, Nar potentiated the MTX effect on the Bax/Bcl-2 ratio. In conclusion, Nar decreased MTX-induced functional and ultrastructural liver damage in a tumor-free animal model. Also, our data introduce MTX and Nar as promising antiproliferative agents with a distinctive mode of action, inducing apoptosis in HepG2 tumor cells through activation of Bax and down-regulation of Bcl-2 protein expression.

a-cypermethrin is one of the most potent insecticides used worldwide. This study was planned to evaluate the possible role of a-lipoic acid in a-cypermethrin induced toxicity in rats. The treated groups were; the control, α-cypermethrin, a-lipoic acid and a-cypermethrin, and a-lipoic acid groups. Our results showed that administration of a-cypermethrin caused a significant decrease in RBC count, PCV, and Hb content and an increase in WBC count. Also, a- cypermethrin caused a significant increase in the levels of cholesterol, TGs, LDL-Cand VLDL-C, while the HDL-C was decreased. Also, a-cypermethrin caused a reduction in serum testosterone, FSH, and LH levels in intoxicated rats. Furthermore, the co-administration of a-lipoic acid mitigated the toxicity of a-cypermethrin by partially normalizing these biochemical parameters. Our results were supported by histopathological observations of the testis. Our data suggest that a-lipoic acid may have a protective role against a-cypermethrin induced toxicity in rats.

Lead is one of the oldest environmental and occupational toxins. Health hazards from increased lead exposure as a result of industrial and environmental pollution are recognized. The aim of the present study was to investigate the protective effects of quercetin as a model of an antioxidant drug against the toxic effects of lead acetate on the blood and the testis of rats. The lead concentrations were determined in blood and the testis. Testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were assessed in serum. Hemoglobin (Hb) content, packed cell volume (PCV), white blood cell (WBC) and red blood cell (RBC) counts were evaluated in the whole blood. Our results showed that administration of lead acetate was associated with an increased lead levels in blood as well as in the testis. Lead acetate administration also caused a decrease in testicular function, Hb content, PCV and RBC count in comparison to the respective mean values of the control. In addition, lead acetate increased WBC count and induced alterations in sperm count, sperm motility and sperm abnormality and histopathology. In the contrary, administration of lead acetate along with quercetin partially restored the studied parameters to normal values. In conclusion, the treatment with quercetin may provide a partial protection against the toxic effects induced by lead acetate in blood and the testis of rats.

The aim of this study was to evaluate the probable protective effect of quercetin (QUE) against cadmium (Cd)-induced sub-chronic toxicity in rats. Adult male rats were given either Cd (as cadmium chloride; 5 mg/kg) alone or in combination with QUE (50 mg/kg) daily for 4 weeks by oral gavage. At the end of the experimental period, Cd accumulation, and selected hematological, thyroid, and reproductive markers were assessed. Results revealed that Cd treatment significantly increased Cd concentrations in blood, thyroid gland, and testicular tissue of rats. Cd also caused a decline in hemoglobin content, hematocrit value, and total erythrocyte and leucocyte counts. Further, significant suppressions in the blood levels of hormones related to thyroid gland function, and male reproductive hormones (i.e., testosterone, luteinizing hormone and follicle-stimulating hormone), were observed in Cd-treated rats compared to the control. In parallel, low sperm count and sperm motility, increased sperm abnormalities, and marked pathology occurred in testis. Combination with QUE recorded amelioration of the deleterious effects of Cd, involving regulation of hematological toxicity and thyroid hormonal levels and subsequently modulation of testicular function. In conclusion, it appears that dietary QUE can rescue from Cd-induced hematological dysfunctions and testicular damage by reversing the hypothyroid state.

The present work aims to evaluatethe cytotoxic effects on lung cells exerted by gasoline. 60 male albino mice were used in the present experiment, divided equally into 3 groups: first group (control) was left access to fresh air, second group (experimental) was subjected to gasoline 80- vapor/1h./day and third group (experimental) was subjected to gasoline 90-vapor/1h./day along eight consecutive weeks. The study comprises determination of body weight, bioaccumulation of some heavy metals ,histological and ultra-changes . Histological changes increased according to duration of exposure as, infiltration of inflammatory cells, detachment and necrosis of the epithelial cells .The electron micrographs revealed dilatation of the smooth endoplasmic reticulum, loss of the secretory granules in the Clara cells and loss of cilia in the ciliated cells that exhibited bleb formation. Necrotic type II pneumocytes, exhibited vacuolation, fragmentation of the rough endoplasmic reticulum,mitochondrial degeneration , nuclear alterations, degeneration of lamellar bodies and microvillar atrophy. In conclusion, gasoline vapour inhalation induced lung tissue injury and cellular damage concomitant with impairment of the lung antioxidant defense system. These effects were more pronounced with the unleaded than with the leaded gasoline.

Rutin, a food derived-polyphenolic bioflavonoid, has been acknowledged for several health benefits. This study aims to explore the ameliorative effects of rutin against carbon tetrachloride (CCl4) toxicity in male rats. Adult male rats were given either CCl4 (30% in olive oil, 3 ml/kg b.w. intraperitoneally) alone or in combination with rutin (70 mg/kg intragastrically) twice a week for 4 weeks. Our data showed that rutin mitigated CCl4 hepatorenal damage, as indicated by diagnostic markers (i.e., transaminases, alkaline phosphatase, total bilirubin, total protein, albumin, urea, uric acid and creatinine), and histopathological findings. In addition, CCl4 induced profound elevation of free radical generation and oxidative stress, as evidenced by increasing lipid peroxidation and reducing catalase, superoxide dismutase and glutathione peroxidase activities in liver, kidney and testicular tissues; these effects were suppressed by coexposure with rutin. Moreover, the increase in the levels of serum triglycerides, cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol induced by CCl4 was effectively counteracted by rutin. The decrease in the level of high-density lipoprotein cholesterol in the CCl4 group was also counteracted by rutin treatment. Interestingly, the decreased levels of hormonal mediators associated with sperm production, including serum testosterone, luteinizing hormone and follicle-stimulating hormone, and the impaired sperm quality induced by CCl4 were reversed by rutin. Data from the current study clearly demonstrated that rutin supplementation could at least partly overcome CCl4-induced hepatotoxicity, nephrotoxicity and reproductive toxicity by antioxidant and antidyslipidemic effects.