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Butylparaben (BuP) is a ubiquitous preservative in cosmetics, foods, and medicine. As an emerging pollutant, it has gained wide attention in recent years. Because amphibians have both aquatic and terrestrial life stages and high skin permeability, they are sensitive to environmental changes. To assess the toxic effects of BuP on amphibians, the present study was conducted on the spot-legged tree frog (Polypedates megacephalus) tadpoles. In the present study, LC50 of BuP for 96 h exposures was 3509 µg/L. Then, the tadpoles were exposed to 0, 350 and 2100 µg/L BuP (hereafter named as CK, B1 and B2) for 12, 24 and 48 h, the oxidative stress and apoptosis in the liver were analyzed. The results showed that the content of MDA and activity of SOD and GSH-PX were increased with an increase in BuP exposure. BuP stress significantly altered the expression of Nrf2-Keap1 signal pathway genes. An increase in the expression of JAK-STAT signal pathway genes was observed with an increase in the exposure to BuP concentration at 24 and 48 h. In contrast, the expression of negative regulators of JAK-STAT signal pathway were significantly increased at 12 h and decreased at 24 and 48 h. A significant decrease in pro-apoptosis genes expression (Bax and Caspase3) were observed at 12 h but increased at 24 and 48 h, while the expression of anti-apoptosis gene (Bcl-2) decreased at 24 and 48 h. These results provide a valuable reference point for assessing the ecological and health risks associated with BuP in the environment. [ABSTRACT FROM AUTHOR]

Butylparaben (BP), a common chemical preservative in cosmetic and pharmaceutical products, has been known to induce oxidative stress and disrupt endocrine function in humans. In contrast, morin, a flavonoid derived from the Moraceae family, exhibits diverse pharmacological properties, including anti‐inflammatory and antioxidant. Despite this, the protective role of morin against oxidative stress‐induced damage in pancreatic islets remains unclear. Therefore, in this study, we aimed to investigate the potential protective mechanism of morin against oxidative stress‐induced damage caused by BP in zebrafish larvae. To achieve this, we exposed the zebrafish larvae to butylparaben (2.5 mg/L) for 5 days, leading to increased oxidative stress and apoptosis in β‐cells. However, our compelling findings revealed that pretreatment with various concentrations of morin effectively reduced mortality and mitigated apoptosis and lipid peroxidation in β‐cells induced by BP exposure. In addition, zebrafish larvae exposed to BP for 5 days exhibited evident β‐cell damage. However, the pretreatment with morin showed promising effects by promoting β‐cell proliferation and lowering glucose levels. Furthermore, gene expression studies indicated that morin pretreatment normalized PEPCK expression while increasing insulin expression in BP‐exposed larvae. In conclusion, our findings highlight the potential of morin as a protective agent against BP‐induced β‐cell damage in zebrafish larvae. The observed improvements in oxidative stress, apoptosis, and gene expression patterns support the notion that morin could be further explored as a therapeutic candidate to counteract the detrimental effects of BP exposure on pancreatic β‐cells. [ABSTRACT FROM AUTHOR]

Due to Butylparaben (BuP) widespread application in cosmetics, food, pharmaceuticals, and its presence as an environmental residue, human and animal exposure to BuP is common, potentially posing hazards to both human and animal health. Congenital heart disease is already a serious problem. However, the effects of BuP on the developing heart and its underlying mechanisms remain unclear. Here, zebrafish embryos were exposed to environmentally and human-relevant concentrations of BuP (0.6 mg/L, 1.2 mg/L, and 1.8 mg/L, calculated but not measured) at 6 h post-fertilization (hpf) and were treated until 72 hpf. Exposure to BuP led to cardiac morphological defects and cardiac dysfunction in zebrafish embryos, manifesting symptoms similar to systolic heart failure. The etiology of BuP-induced systolic heart failure in zebrafish embryos is multifactorial, including cardiomyocyte apoptosis, endocardial and atrioventricular valve damage, insufficient myocardial energy, impaired Ca2+ homeostasis, depletion of cardiac-resident macrophages, cardiac immune non-responsiveness, and cardiac oxidative stress. However, excessive accumulation of reactive oxygen species (ROS) in the cardiac region and cardiac immunosuppression (depletion of cardiac-resident macrophages and cardiac immune non-responsiveness) may be the predominant factors. In conclusion, this study indicates that BuP is a potential hazardous substance that can cause adverse effects on the developing heart and provides evidence and insights into the pathological mechanisms by which BuP leads to cardiac dysfunction. It may help to prevent the BuP-based congenital heart disease heart failure in human through ameliorating strategies and BuP discharge policies, while raising awareness to prevent the misuse of preservatives.

BACKGROUND: Most studies have focused on the degradation of endocrine‐disrupting chemicals using persulfate activation processes. Therefore, the current study compares various sulfate radical activation processes in an aqueous solution of a mixture of diethyl phthalate, butylparaben and bisphenol A that are present in water and wastewater. The effects of initial persulfate dose and pH variation, the effect of concentration of target endocrine‐disrupting chemicals and degradation efficiency under various processes were studied. Additionally, the toxicity and cost estimation of the systems were also examined. RESULTS: The results showed pseudo‐first‐order kinetics with maximum degradation efficiency of 99% for 1 mg L−1 at pH 7, 2.5 mmol L−1 persulfate dose, 450 W power in 60 min for UV‐activated persulfate oxidation process. A quenching experiment highlights the dominance of both sulfate and hydroxyl radicals in the degradation of mixtures of diethyl phthalate, butylparaben and bisphenol A in an aqueous solution. The transformative products identified using gas chromatography–mass spectrometry were monohydroxylated structures that decompose to form organic acids, indicating efficient degradation capacity with minimal toxicity. Further, the sono‐activated persulfate oxidation process was found to be cost‐effective at 1 mg L−1 with 95% degradation efficiency. CONCLUSION: It is concluded that an increase in the concentration of target compounds decreases the efficiency of degradation under various activation processes. pH 3 and pH 7 favor thermal and sono‐activated and UV‐activated processes, respectively. Toxicity evaluation shows minimal harm to non‐target species Daphnia magna for all activation processes. These findings can be useful for on‐field application for the degradation of chemicals in mixtures. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Butylparaben is an ubiquitous environmental endocrine disruptor, that is commonly used in cosmetics and personal care product due to its anti-microbial properties. Butylparaben has been shown to cause developmental toxicity, endocrine and metabolic disorders and immune diseases. However, little is known about the impact on female fertility, especially oocyte quality. In the present study, we reported that butylparaben influenced female fertility by showing the disturbed oocyte meiotic capacity and fertilization potential. Specifically, butylparaben results in the oocyte maturation arrest by impairing spindle/chromosome structure and microtubule stability. Besides, butylparaben results in fertilization failure by impairing the dynamics of Juno and ovastacin and the sperm binding ability. Last, single-cell transcriptome analysis showed that butylparaben-induced oocyte deterioration was caused by mitochondrial dysfunction, which led to the accumulation of ROS and occurrence of apoptosis. Collectively, our study indicates that mitochondrial dysfunction and redox perturbation is the major cause of the weakened female fertility expoesd to butylparaben.

Butylparaben (BuP) is a common antibacterial preservative utilized extensively in food, medical supplies, cosmetics, and personal care products. The current study reports the use of Zebrafish (Danio rerio) embryos to investigate potential developmental toxicity caused by exposure to BuP. The development of Neural crest cells (NCCs) is highly active during gastrulation in Zebrafish embryos. Thus, we utilized 0.5 mg/L, 0.75 mg/L, and 1 mg/L BuP solutions, respectively, in accordance with the international safety standard dosage. We observed severe craniofacial cartilage deformities, periocular edema, cardiac dysplasia, and delayed otolith development in the Zebrafish larvae 5 days after exposure. The oxidative stress response was significantly enhanced. In addition, the biochemical analysis revealed that the activities of catalase (CAT) and superoxide dismutase (SOD) were significantly reduced relative to the control group, whereas the concentration of malondialdehyde (MDA) was significantly elevated. Furthermore, ALP activity, a marker of osteoblast activity, was also reduced. Moreover, the RT-qPCR results indicated that the expression of chondrocyte marker genes sox9a, sox9b, and col2a1a was down-regulated. In addition, the morphology of maxillofacial chondrocytes was altered in Zebrafish larvae, and the proliferation of cranial NCCs was inhibited. Accordingly, our findings indicate that strong oxidative stress induced by BuP inhibits the proliferation of NCCs in larval Zebrafish, leading to craniofacial deformities.

Pesticides and personal care products are two very important groups of contaminants posing a threat to the aquatic environment and the organisms living in it.. Therefore, this study aimed to describe the effects of widely used pesticides and parabens on aquatic non-target biota such as fish (using model organisms Danio rerio and Cyprinus carpio) and amphibians (using model organism Xenopus laevis) using a wide range of endpoints. The first part of the experiment was focused on the embryonal toxicity of three widely used pesticides (metazachlor, prochloraz, and 4-chloro-2-methyl phenoxy acetic acid) and three parabens (methylparaben, propylparaben, and butylparaben) with D. rerio, C. carpio, and X. laevis embryos. An emphasis was placed on using mostly sub-lethal concentrations that are partially relevant to the environmental concentrations of the substances studied. In the second part of the study, an embryo-larval toxicity test with C. carpio was carried out with prochloraz using concentrations 0.1, 1, 10, 100, and 1000 µg/L. The results of both parts of the study show that even the low, environmentally relevant concentrations of the chemicals tested are often able to affect the expression of genes that play either a prominent role in detoxification and sex hormone production or indicate cell stress or, in case of prochloraz, to induce genotoxicity. [ABSTRACT FROM AUTHOR]

Parabens are group of preservatives chemical compounds used in cosmetics, personal hygiene product, food products and pharmaceuticals. In this study the hepatorenal toxicity due to exposure to paraben was evaluated. In this study design Twenty four of albino rats experimentally used. Butyle paraben (BP) orally was given to animals 180 days in dose of 4.6 mg\kg.bw which equal to10 % of the LD50 of BP. The extract of Mushroom was given by stomach tube in dose of 10 mg/kg/day for six 180 days. Exposure to Parabens exhibited histopathological and biochemical alterations. In the line of biochemical analysis BP induced toxic changes in both liver and kidney, the hepatic cellular enzymes concentrations (AST, ALT), Bilirubin, urea and creatinine were raised. In contrast plasma proteins were decreased in comparison to the control group. In renal and hepatic tissues BP administration induced vascular congestion as well as necrosis in the hepatorenal epithelium. Both the biochemical and histopathological alteration was improved after giving mushroom extracts in comparison to BP given group. In conclusion, mushroom extracts exhibited biochemical and histopathological improvement in liver and kidney against the toxicity by Butylparaben.

Alkylphenols can originate from numerous products containing alkylphenol ethoxylates, including cleaning products, household items, and cosmetics. Some phenols, such as nonylphenol, are known to be endocrine disruptors, and exposure to them is thought to have contributed to the recent increase in allergic diseases such as asthma. However, the impacts of prenatal phenol exposure on asthma development in children are still unclear. We analyzed the association between maternal urinary phenol concentrations during early pregnancy and the development of asthma in children at the age of 4, using data from the Japan Environment and Children's Study (JECS), a large-scale nationwide birth cohort study. We recruited 3,513 pairs of mothers and children participating in the Sub-Cohort Study of JECS. We measured 24 phenols, including nitrophenol, parabens, bisphenol, octylphenol, and nonylphenol, in urine samples taken during the first trimester of pregnancy. The urinary levels of these phenols differed markedly, and some showed a broad spectrum of distribution. Methylparaben was detected at high levels in almost every participant (267.7 ng/ml, standard deviation 433.78). Logistic regression analysis revealed that the odds ratio of asthma onset for high exposure to butylparaben was 1.54 (95% confidence interval: 1.11–2.15). Additionally, logistic regression analysis by gender revealed an asthma development odds ratio of 2.09 (95% confidence interval: 1.20–3.65) for males and 0.65 (95% confidence interval: 0.25–1.70) for females born to mothers in whom 4-nonylphenol was detected, suggesting a gender difference. Our current analysis using large cohort data suggests that high exposure to butylparaben and low exposure to 4-nonylphenol during pregnancy are risk factors for asthma development in children. These findings establish a valuable foundation for formulating recommendations about prenatal phenol exposure. [Display omitted] • 3,513 mother-child pairs were analyzed for the association between phenol and asthma. • Total of 24 phenols were measured in urine samples collected from pregnant mothers. • Children born to mothers with high butylparaben had a higher risk of asthma. • Male children born to mothers with 4-nonylphenol had a higher risk of asthma. [ABSTRACT FROM AUTHOR]

The presence of butylparaben (BP), a prevalent pharmaceutical and personal care product, in surface waters has raised concerns regarding its impact on aquatic ecosystems. Despite its frequent detection, the toxicity of BP to the cyanobacterium Microcystis aeruginosa remains poorly understood. This study investigates the influence of BP on the growth and physiological responses of M. aeruginosa. Results indicate that low concentrations of BP (below 2.5 mg/L) have negligible effects on M. aeruginosa growth, whereas higher concentrations (5 mg/L and 10 mg/L) lead to significant growth inhibition. This inhibition is attributed to the severe disruption of photosynthesis, evidenced by decreased Fv/Fm values and chlorophyll a content. BP exposure also triggers the production of reactive oxygen species (ROS), resulting in elevated activity of antioxidant enzymes. Excessive ROS generation stimulates the production of microcystin-LR (MC-LR). Furthermore, lipid peroxidation and cell membrane damage indicate that high BP concentrations cause cell membrane rupture, facilitating the release of MC-LR into the environment. Transcriptome analysis reveals that BP disrupts energy metabolic processes, particularly affecting genes associated with photosynthesis, carbon fixation, electron transport, glycolysis, and the tricarboxylic acid cycle. These findings underscore the profound physiological impact of BP on M. aeruginosa and highlight its role in stimulating the production and release of MC-LR, thereby amplifying environmental risks in aquatic systems. [Display omitted] • A high dose of butylparaben modified the cell membrane integrity of M. aeruginosa. • Butylparaben disrupted photosynthesis and induced oxidative stress. • A high dose of butylparaben increased microcystin-LR secretion. • The molecular mechanism of M. aeruginosa to butylparaben was provided. [ABSTRACT FROM AUTHOR]

Parabens (PBs) are commonly utilized as preservatives in various commodities. Of all the PBs, methylparaben (MeP) and butylparaben (BuP) are usually found together at similar levels in the aqueous environment. Although a few studies have demonstrated that PBs are neurotoxic when present alone, the neurobehavioral toxic effects and mechanisms of coexisting MeP and BuP at environmental levels has not been determined. Neurobehavior is a sensitive indicator for identifying neurotoxicity of environmental pollutants. Therefore, adult female zebrafish (Danio rerio) were chronic co-exposure of MeP and BuP at environmental levels (5, 50, and 500 ng/L) for 60 d to investigate the effects on neurobehavior, histopathology, oxidative stress, mitochondrial function, neurotransmitters and gene expression. The results demonstrated that chronic co-exposure of MeP and BuP interfered with several behaviors (learning-memory, anxiety, fear, aggressive and shoaling behavior) in addition to known mechanisms of producing oxidative stress and disrupting energy. More intriguingly, chronic co-exposure of MeP and BuP caused retinal vacuolization and apoptosis in the optic tectum zone. It even has further effects on the phototransduction pathway, impairing optesthesia and leading to neurotransmitters dysregulation. These are critical underlying mechanisms resulting in neurobehavioral abnormalities. This study confirms that the pollution of multiple PBs by chronic co-exposure in aquatic environments can result neurobehavioral toxicity. It also suggests that the prolonged effects of PBs on aquatic ecosystems and health require close attention. [Display omitted] • Coexistence of multiple parabens is frequently observed in aquatic environments. • Combined methylparaben and butylparaben altered neurobehaviors in adult zebrafish. • Combined methylparaben and butylparaben disrupted optesthesia and neurotransmitters. • Neurobehavioral toxicity linked to combined parabens requires careful consideration. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate potential genotoxic effects in blood and liver samples of male rats of pubertal age following the administration of butylparaben (BP). Materials and Methods: A total of 48 6-week-old male rats were divided randomly into 8 equal groups. Three groups received 200, 400, or 800 mg/kg/day BP for 14 days; 3 groups received 100, 200, or 400 mg/kg/day for 28 days; and 2 control groups received corn oil or methyl methanesulfonate. Blood and liver samples were analyzed to determine any genotoxic effect using comet assay parameters of tail moment, tail length, and tail intensity. Results: Significant differences were observed between the control and treatment groups: liver sample analysis revealed that the tail length of the 28-day dose groups was lower than that of the 14-day dose groups and some tail moment and the tail intensity values were high in the BP treatment groups. The measurements of tail length in the 200 and 400 mg/kg/day BP groups was higher than that of the control groups, while in the 800 mg/kg/day group, it was lower than that of the control group. The lymphocyte values in the 14-day high-dose groups were higher than the 28-day low-dose data. Conclusion: The results indicated that BP had genotoxic potential in the blood and liver cells of young male rats. [ABSTRACT FROM AUTHOR]

Butylparaben, a common preservative, is widely used in food, pharmaceuticals and personal care products. Epidemiological studies have revealed the close relationship between butylparaben and diabetes; however the mechanisms of action remain unclear. In this study, we administered butylparaben orally to mice and observed that exposure to butylparaben induced glucose intolerance and hyperlipidemia. RNA sequencing results demonstrated that the enrichment of differentially expressed genes was associated with lipid metabolism, bile acid metabolism, and inflammatory response. Western blot results further validated that butylparaben promoted hepatic lipogenesis, inflammation, gluconeogenesis, and insulin resistance through the inhibition of the farnesoid X receptor (FXR) pathway. The FXR agonists alleviated the butylparaben-induced metabolic disorders. Moreover, 16 S rRNA sequencing showed that butylparaben reduced the abundance of Bacteroidetes , S24–7, Lactobacillus, and Streptococcus , and elevated the Firmicutes / Bacteroidetes ratio. The gut microbiota dysbiosis caused by butylparaben led to decreased bile acids (BAs) production and increased inflammatory response, which further induced hepatic glycolipid metabolic disorders. Our results also demonstrated that probiotics attenuated butylparaben-induced disturbances of the gut microbiota and hepatic metabolism. Taken collectively, the findings reveal that butylparaben induced gut microbiota dysbiosis and decreased BAs production, which further inhibited FXR signaling, ultimately contributing to glycolipid metabolic disorders in the liver. [Display omitted] • Butylparaben induces glycolipid metabolic disorder and gut microbiota dysbiosis. • Butylparaben disturbs metabolic homeostasis via gut microbiota and FXR pathway. • FXR agonists and probiotics can ameliorate the disturbances caused by butylparaben. [ABSTRACT FROM AUTHOR]

Pesticides and personal care products are two very important groups of contaminants posing a threat to the aquatic environment and the organisms living in it.. Therefore, this study aimed to describe the effects of widely used pesticides and parabens on aquatic non-target biota such as fish (using model organisms Danio rerio and Cyprinus carpio) and amphibians (using model organism Xenopus laevis) using a wide range of endpoints. The first part of the experiment was focused on the embryonal toxicity of three widely used pesticides (metazachlor, prochloraz, and 4-chloro-2-methyl phenoxy acetic acid) and three parabens (methylparaben, propylparaben, and butylparaben) with D. rerio, C. carpio, and X. laevis embryos. An emphasis was placed on using mostly sub-lethal concentrations that are partially relevant to the environmental concentrations of the substances studied. In the second part of the study, an embryo-larval toxicity test with C. carpio was carried out with prochloraz using concentrations 0.1, 1, 10, 100, and 1000 µg/L. The results of both parts of the study show that even the low, environmentally relevant concentrations of the chemicals tested are often able to affect the expression of genes that play either a prominent role in detoxification and sex hormone production or indicate cell stress or, in case of prochloraz, to induce genotoxicity.

Butylparaben is an organic compound that is used as an antimicrobial preservative in cosmetics and can cause neurotoxicity. However, whether butylparaben induces neuronal death is unclear. In this study, we report that butylparaben exposure induced neuronal apoptosis mediated by ER stress in primary cortical neurons. We found that butylparaben significantly inhibited the viability of primary cortical neurons and led to lactate dehydrogenase (LDH) release from primary cortical neurons. Upon exposure to butylparaben, primary cortical neurons exhibited increased levels of apoptosis-related proteins such as Cleaved-caspase3 and Bax. Interestingly, butylparaben-induced activation of apoptosis involved the upstream activation of ER stress proteins such as GRP78, CHOP, and ATF4. However, pharmacological inhibition of ER stress prevented the butylparaben-induced induction of apoptosis. Taken together, our findings suggest that butylparaben exposure activates the ER stress-mediated apoptosis of primary cortical neurons, which is closely linked with neurodegeneration in the brain. Therefore, targeting ER stress may be considered a strategy for the treatment of butylparaben-induced neurodegeneration. [ABSTRACT FROM AUTHOR]

Parabens are classified as endocrine disrupting chemicals due to their ability to activate several nuclear receptors causing changes in hormones‐dependent signalling pathways. Central nervous system of developing organisms is particularly vulnerable to changes in hormonal pathways, which could lead to altered brain function, abnormal behaviour and even diseases later in life. The aim of the present study was to investigate the effects of exposure to butylparaben (BuP), ethylparaben (EtP) and methylparaben (MeP) during early development on nervous system using zebrafish larvae's behavioural models. Zebrafish were exposed until 4 days post fertilization (dpf) to three concentrations of each paraben chosen considering the environmentally realistic concentrations of human exposure and the benchmark‐dose lower bound calculated for zebrafish larvae (BuP: 5, 50 and 500 μg/L; EtP: 50, 500 and 5000 μg/L; MeP: 100, 1000 and 10,000 μg/L). Activity in novel and in familiar environment, thigmotaxis, visual startle response and photic synchronization of the behavioural circadian rhythms were analysed at 4, 5 and 6 dpf. Zebrafish larvae exposed to BuP 500 μg/L and EtP 5000 μg/L revealed increased anxiety‐like behaviour in novel environment. Larvae treated with 500 μg/L of BuP showed reduced activity in familiar and marginally in unfamiliar environment, and larvae exposed to 5000 μg/L of EtP exhibited hyperactivity in familiar environment. Parabens exposure did not influence the visual startle response and the photic synchronization of circadian rhythms in zebrafish larvae. This research highlighted as the exposure to parabens has the potential to interfere with behavioural development of zebrafish. Zebrafish larvae were used as model to study the effects of three parabens (butylparaben, ethylparaben and methylparaben) during early development on zebrafish nervous system. The results suggest the neurotoxic potential of parabens. According to their chemical properties, BuP seems to induce more pronounced behavioural effects than EtP, and in addition, MeP did not produce effects on larvae behaviour. [ABSTRACT FROM AUTHOR]

Parabens are widely used preservatives in cosmetics and pharmaceutical products and are approved as food additives. These chemicals have been considered safe for many years. However, the literature classifies parabens as endocrine-disrupting chemicals, and an assessment of their influence on the endocrine system and systemic toxicity is important. This study explored long-term systemic toxicity, effects on the endocrine system, and toxicokinetic behavior after repeated subcutaneous administration of butylparaben to Sprague–Dawley rats. Rats were treated with vehicle (4% Tween 80) or butylparaben at dose levels of 2, 10, and 50 mg/kg/day for 13 weeks. Assessment of systemic toxicity and endocrine-disrupting effects was based on mortality; clinical signs; body weight; food and water consumption; ophthalmological findings; urinalysis; hematology and clinical biochemistry; organ weights; necropsy and histopathological findings; regularity and length of the estrous cycle; semen quality; and toxicokinetic behavior. Female uterine weight and estrous cycle, and male semen quality indicated no estrogenic effects. Butylparaben induced local irritation at the injection site in both sexes at a dose of 50 mg/kg/day, but systemic toxicity was not observed. Therefore, the no-observed-adverse-effect level of butylparaben is set at 50 mg/kg/day in rats of both sexes. Butylparaben was without endocrine system effects at this dose. Butylparaben displays dose-dependent systemic exposure up to the maximum dose of 50 mg/kg/day and repeated administration of butylparaben for 13 weeks shows no bioaccumulation. [ABSTRACT FROM AUTHOR]

Butylparaben, a common endocrine disruptor in the environment, is known to be toxic to the reproductive system, heart, and intestines, but its nephrotoxicity has rarely been reported. In order to study the nephrotoxicity and mechanism of butylparaben, we examined the acute and chronic effects on human embryonic kidney cells (HEK293T) and zebrafish. Additionally, we assessed the potential remedial effects of salidroside against butylparaben-induced nephrotoxicity. Our in vitro findings demonstrated oxidative stress and cytotoxicity to HEK293T cells caused by butylparaben. In the zebrafish model, the concentration of butylparaben exposure ranged from 0.5 to 15 μM. An assortment of experimental techniques was employed, including the assessment of kidney tissue morphology using Hematoxylin-Eosin staining, kidney function analysis via fluorescent dextran injection, and gene expression studies related to kidney injury, development, and function. Additionally, butylparaben caused lipid peroxidation in the kidney, thereby damaging glomeruli and renal tubules, which resulted from the downregulation of the PI3K-AKT signaling pathway. Furthermore, salidroside ameliorated butylparaben-induced nephrotoxicity through the PI3K-AKT signaling pathway. This study reveals the seldom-reported kidney toxicity of butylparaben and the protective effect of salidroside against toxicological reactions related to nephrotoxicity. It offers valuable insights into the risks to kidney health posed by environmental toxins. [Display omitted] • Butylparaben causes oxidative stress and toxicity in HEK293T cells. • Butylparaben can induce acute kidney injury in zebrafish larvae. • Butylparaben can inflict chronic nephrotoxicity in adult zebrafish. • Salidroside mitigates butylparaben-induced nephrotoxicity, potentially via the PI3K-AKT signaling pathway. [ABSTRACT FROM AUTHOR]

A novel, cheap and easy-to-construct device and a simple method for partition coefficient determination in liposome/water system based on modified equilibrium dialysis have been developed. The device consists of two vials separated by a semi-permeable membrane, through which the free form of a low molecular weight substance is transported by shaking assisted diffusion. Five test substances, eugenol, carvacrol, thymol, 4-hydroxybenzyl alcohol (4-HBA) and butylparaben were analyzed after equilibration in aqueous phase by three methods, HPLC-UV, GC-MS and DPV with comparable results. This shows the possibility of using the proposed method in any laboratory with any equipment capable of analyzing the substance under study. The liposome/water partition coefficients (log P l/w) determined for eugenol (2.39), thymol (2.83), carvacrol (2.78) and butylparaben (3.30) are consistent with previously published data. A strong effect of NaCl on the liposome/water partition coefficient was observed. The value of log P l/w = 1.06 determined for 4-HBA in the presence of 0.15 mol L-1 NaCl in the partitioning liposomal system was considerably lower than in the absence of the salt (log P l/w = 2.06). The developed method was used to determine the partition coefficient of morphine in liposome/water system without NaCl (log P l/w = 2.65) under given conditions. [Display omitted] • Novel device for determination of liposome-water partition coefficient. • Simple, low cost, reusable and eco-friendly design for "green" applications. • Comparison of three types of exchangeable hydrophilic semipermeable membranes. [ABSTRACT FROM AUTHOR]

Mammalian reproduction is a highly regulated process that can be distorted following exposure to synthetic antimicrobial preservatives like butylparaben (BP). Besides, studies have not investigated the potential antioxidant effects of turmeric on BP-provoked reprotoxicity. The present research was planned on prepubertal mice, orally treated with BP (150 μg/g body weight/day) with and without Curcuma longa (turmeric) (400 μg/mice/day) from postnatal day 35 to 65 routinely. Results showed an insignificant reduction in body weight of both sexes but contrary to these, gonadal weight increased significantly in PB-exposed mice. Additionally, elevated levels of follicle-stimulating hormone and luteinizing hormone while decreased estrogen levels were observed in BP-treated females against control. Sperm count and motility were disturbed, coupled with abnormal sperm morphology in BP-intoxicated group. These findings were synchronized with a decreased testosterone levels in the same group as compared with control. The follicular count revealed reduction in the number of antral follicles while an increase in empty follicles. The BP also significantly increased lipid peroxidation and decreased glutathione content, superoxide dismutase, and catalase activities, while the morphometric, biochemical, and histological deviations were less pronounced in the group, which was co-administered with BP and turmeric. Results indicated that turmeric has antioxidant potential to protect BP-induced oxidative stress and reprotoxicity in mice. [ABSTRACT FROM AUTHOR]

• Public safety concerns of endocrine disruption by parabens have been on the rise. • Toxicity was assessed using multigenerational continuous breeding study design. • Increased liver weight and hepatic hypertrophy occurred in perinatally exposed rats. • Reproduction and pubertal development were unperturbed by butylparaben exposure. Butylparaben (BP) is an antimicrobial agent utilized for decades as a preservative in numerous consumer products. The safety of parabens has recently come under scrutiny based on reports of estrogenic activity and suggested adverse effects upon the reproductive system. Due to the limited availability of studies that address the potential for BP exposure to induce reproductive toxicity, and clear evidence of human exposure, the National Toxicology Program conducted a multigenerational continuous breeding study to evaluate the impact of dietary BP-exposure at 0, 5000, 15,000, or 40,000 ppm on reproductive and developmental parameters in Hsd:Sprague Dawley SD rats. BP-exposure was not associated with adverse alterations of fertility, fecundity, pubertal attainment, or reproductive parameters in F0, F1, or F2 generations. Exposure-dependent increases in liver weights, and incidences of non-neoplastic liver lesions suggest the liver is a target organ of BP toxicity. No findings were observed that would support the purported mechanism of BP-induced endocrine disruption in perinatally-exposed rodents. [ABSTRACT FROM AUTHOR]

Anthropogenic chemicals such as parabens and triclosan are used in personal care products. Due to their ability to decrease or prevent bacterial contamination and act as preservatives, these chemicals are used in cosmetic manufacturing processes to increase the shelf life of products. In this study, we assessed the side effects of environmental estrogens (such as the xenoestrogen butylparaben and the antimicrobial agent and preservative triclosan) on thyroid function, brain monoamine levels, and DNA aberration. Forty‐two male albino rats were divided into seven groups with six members each: the first group served as control; the second and the third groups were treated with butylparaben 10 and 50 mg/kg body weight, respectively; the fourth and fifth groups were treated with triclosan 10 and 50 mg/kg body weight, respectively; and the sixth and seventh groups were treated with butylparaben plus triclosan 10 and 50 mg/kg body weight, respectively. After 60 days, blood samples were collected and brain specimens were divided into striatum, midbrain, cortex, and thalamus. Thyroid function and levels of monoamines and monoamine metabolites were determined for each brain area. Comet assay was used for brain tissue analysis. The results showed that butylparaben and triclosan and their combinations induced hypothyroidism and disrupted monoamine levels, leading to a decrease in catecholamine and serotonin levels, and accelerated production of 5‐hydroxyindoleacetic acid. The obtained data indicate that anthropogenic chemicals such as butylparaben and triclosan have harmful effects on thyroid and brain function and accelerate cell destruction and mutation, as evidenced by single‐stranded DNA breaks in the comet assay. [ABSTRACT FROM AUTHOR]

We investigated whether butylparaben supplementation to the culture media negatively effects on in vitro development of mouse preantral follicle. The preantral follicles were isolated from the ovaries of 7–8-week-old mice and cultured in growth medium for 10 days and then in maturation medium for 2 days. During in vitro culture, butylparaben (0, 0.01, 0.1, 1.0, or 10 μM) was supplemented to the culture media. In the final spent media, the levels of 17ß-estradiol and anti-Müllerian hormone (AMH) were measured via enzyme-linked immunosorbent assay. In the final luteinized follicular cells, the mRNA levels of steroidogenic acute regulatory protein (StAR), superoxide dismutase 1 (Sod1), caspase 3 (Casp3), and extracellular signal-regulated kinase 1 (Erk1) were quantified via real-time reverse transcription-polymerase chain reaction. The metaphase II oocyte acquisition (per total oocyte) tended to decrease in the four butylparaben-supplemented groups, but not significant (26.8%, 23.2%, 21.4%, 15.1%, and 16.8%, respectively). The level of 17ß-estradiol and AMH tended to decrease in all butylparaben-supplemented groups, but statistically not significant. The expression level of StAR and Erk1 mRNA was significantly higher in all four butylparaben-supplemented groups, and a dose-dependent increment tendency was observed. Our findings suggest that butylparaben supplementation has largely no impact on in vitro development of mouse preantral follicle as well as 17ß-estradiol and AMH production. However, StAR, Sod1, Casp3, and Erk1 genes could be overexpressed in a certain concentration of butylparaben. [ABSTRACT FROM AUTHOR]

In cosmetics and food products, parabens are widely used as antimicrobial agents. Reports have suggested that parabens may be linked to infertility, owing to their effects on basal steroidogenesis properties or their capacity to inflict mitochondrial damage. Despite growing concerns about parabens as endocrine disruptors, it is unclear whether they affect any of these actions in humans, particularly at environmentally relevant concentrations. In this work, an in vitro primary culture of human granulosa cells was used to evaluate steroidogenesis, based on the assessment of progesterone production and regulation of critical steroidogenic genes: CYP11A1, HSD3B1, CYP19A1, and HSD17B1. The effects of two commercially relevant parabens, methylparaben (MPB) and butylparaben (BPB), were screened. Cells were exposed to multiple concentrations ranging from relatively low (typical environmental exposure) to relatively high. The effect was assessed by the parabens' ability to modify steroidogenic genes, progesterone or estradiol production, and on mitochondrial health, by evaluating mitochondrial activity as well as mtDNA content. Neither MPB nor BPB showed any effect over progesterone production or the expression of genes controlling steroid production. Only BPB affected the mitochondria, decreasing mtDNA content at supraphysiological concentrations (1000 nM). Prolonged exposure to these compounds produced no effects in neither of these parameters. In conclusion, neither MPB nor BPB significantly affected basal steroidogenesis in granulosa cells. Although evidence supporting paraben toxicity is prevalent, here we put forth evidence that suggests that parabens do not affect basal steroidogenesis in human granulosa cells. [ABSTRACT FROM AUTHOR]

Due to Butylparaben (BuP) widespread application in cosmetics, food, pharmaceuticals, and its presence as an environmental residue, human and animal exposure to BuP is common, potentially posing hazards to both human and animal health. Congenital heart disease is already a serious problem. However, the effects of BuP on the developing heart and its underlying mechanisms remain unclear. Here, zebrafish embryos were exposed to environmentally and human-relevant concentrations of BuP (0.6 mg/L, 1.2 mg/L, and 1.8 mg/L, calculated but not measured) at 6 h post-fertilization (hpf) and were treated until 72 hpf. Exposure to BuP led to cardiac morphological defects and cardiac dysfunction in zebrafish embryos, manifesting symptoms similar to systolic heart failure. The etiology of BuP-induced systolic heart failure in zebrafish embryos is multifactorial, including cardiomyocyte apoptosis, endocardial and atrioventricular valve damage, insufficient myocardial energy, impaired Ca2+ homeostasis, depletion of cardiac-resident macrophages, cardiac immune non-responsiveness, and cardiac oxidative stress. However, excessive accumulation of reactive oxygen species (ROS) in the cardiac region and cardiac immunosuppression (depletion of cardiac-resident macrophages and cardiac immune non-responsiveness) may be the predominant factors. In conclusion, this study indicates that BuP is a potential hazardous substance that can cause adverse effects on the developing heart and provides evidence and insights into the pathological mechanisms by which BuP leads to cardiac dysfunction. It may help to prevent the BuP-based congenital heart disease heart failure in human through ameliorating strategies and BuP discharge policies, while raising awareness to prevent the misuse of preservatives. [Display omitted] • BuP can cause zebrafish embryonic systolic heart failure. • BuP damages cardiac-resident macrophages in zebrafish embryos. • BuP impairs the cardiac immune response in zebrafish embryos. • Endocardial defects induced by BuP are related to the downregulation of klf2a. • The ROS caused by BuP mainly accumulate in the zebrafish embryo heart region. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the kinetics of methylparaben (MPB) and butylparaben (BPB) removal, two emerging pollutants with possible endocrine disrupting effects, from agricultural soil with and without amendment with compost from sewage sludge used as biostimulant. Compound removal is explained by a first-order kinetic model with half-life times of 6.5/6.7 days and 11.4/8.2 days, in presence/absence of compost, for MPB and BPB respectively. % R2 for the fitted model were higher than 96% in all cases. Additionally, isolation of bacteria capable to grow using MPB or BPB as carbon source was also carry out. Laboratory tests demonstrated the ability of these bacteria to biodegrade MPB and BPB from culture media in more than 95% in some cases. These strains showed high ability to biodegrade the compounds. Ten isolates, most of them related to Gram positive bacteria of the genus Bacillus , were identified by 16S rRNA gene sequencing. The study of the enzymatic activities of the isolates revealed both esterase (C4) and esterase-lipase activities. • Removal of methyl and butylparabens was investigated in soil and amended soil. • Bacteria able to biodegrade methyl and butylparabens were isolated from soils. • Most isolates using parabens as carbon source were related to Bacillus. • All bacterial isolates displayed esterase (C4) and esterase lipase enzyme activities. [ABSTRACT FROM AUTHOR]

Butylparaben is an ubiquitous environmental endocrine disruptor, that is commonly used in cosmetics and personal care product due to its anti-microbial properties. Butylparaben has been shown to cause developmental toxicity, endocrine and metabolic disorders and immune diseases. However, little is known about the impact on female fertility, especially oocyte quality. In the present study, we reported that butylparaben influenced female fertility by showing the disturbed oocyte meiotic capacity and fertilization potential. Specifically, butylparaben results in the oocyte maturation arrest by impairing spindle/chromosome structure and microtubule stability. Besides, butylparaben results in fertilization failure by impairing the dynamics of Juno and ovastacin and the sperm binding ability. Last, single-cell transcriptome analysis showed that butylparaben-induced oocyte deterioration was caused by mitochondrial dysfunction, which led to the accumulation of ROS and occurrence of apoptosis. Collectively, our study indicates that mitochondrial dysfunction and redox perturbation is the major cause of the weakened female fertility expoesd to butylparaben. [Display omitted] • BP affects female reproductive system and the hypothalamus-pituitary-ovarian axis. • Disrupted sexual hormone levels alter ovarian reserve function after BP exposure. • The maturation of the nucleus and cytoplasm was disrupted in BP-exposed oocytes. • BP reduces female fertility by impairing the fertilization potential of oocytes. • BP promotes ROS accumulation and DNA damage to induce early apoptosis in oocytes. [ABSTRACT FROM AUTHOR]

Butylparaben (BuP) is a common antibacterial preservative utilized extensively in food, medical supplies, cosmetics, and personal care products. The current study reports the use of Zebrafish (Danio rerio) embryos to investigate potential developmental toxicity caused by exposure to BuP. The development of Neural crest cells (NCCs) is highly active during gastrulation in Zebrafish embryos. Thus, we utilized 0.5 mg/L, 0.75 mg/L, and 1 mg/L BuP solutions, respectively, in accordance with the international safety standard dosage. We observed severe craniofacial cartilage deformities, periocular edema, cardiac dysplasia, and delayed otolith development in the Zebrafish larvae 5 days after exposure. The oxidative stress response was significantly enhanced. In addition, the biochemical analysis revealed that the activities of catalase (CAT) and superoxide dismutase (SOD) were significantly reduced relative to the control group, whereas the concentration of malondialdehyde (MDA) was significantly elevated. Furthermore, ALP activity, a marker of osteoblast activity, was also reduced. Moreover, the RT-qPCR results indicated that the expression of chondrocyte marker genes sox9a, sox9b, and col2a1a was down-regulated. In addition, the morphology of maxillofacial chondrocytes was altered in Zebrafish larvae, and the proliferation of cranial NCCs was inhibited. Accordingly, our findings indicate that strong oxidative stress induced by BuP inhibits the proliferation of NCCs in larval Zebrafish, leading to craniofacial deformities. • BuP can cause developmental toxicity and craniofacial deformities in zebrafish. • BuP inhibits the proliferation of neural crest cells. • Craniofacial deformities caused by BuP is related to oxidative stress. • BuP injures the craniofacial bone development of non-target species. [ABSTRACT FROM AUTHOR]

Parabens are widely used in personal care products due to their antimicrobial effects. Although the toxicity of parabens has been reported, little information is available on the toxicity of butylparaben (BP) on oocyte maturation. Therefore, we investigated the effects of various concentrations of BP (0 μM, 100 μM, 200 μM, 300 μM, 400 μM, and 500 μM) on the in vitro maturation of porcine oocytes. BP supplementation at a concentration greater than 300 μM significantly reduced the proportion of complete cumulus cell expansion and metaphase II oocytes compared to the control. The 300 μM BP significantly decreased fertilization, cleavage, and blastocyst formation rates with lower total cell numbers and a higher rate of apoptosis in blastocysts compared to the control. The BP-treated oocytes showed significantly higher reactive oxygen species (ROS) levels, and lower glutathione (GSH) levels than the control. BP significantly increased the aberrant mitochondrial distribution and decreased mitochondrial function compared to the control. BP-treated oocytes exhibited significantly higher percentage of γ-H2AX, annexin V-positive oocytes and expression of LC3 than the control. In conclusion, we demonstrated that BP impaired oocyte maturation and subsequent embryonic development, by inducing ROS generation and reducing GSH levels. Furthermore, BP disrupted mitochondrial function and triggered DNA damage, early apoptosis, and autophagy in oocytes.

Abstract: The effect of treatment with combined butylparaben and triclosan on male gonadal toxicity in weanling rats was investigated. All treated groups experienced atrophy in the ventral prostate and seminal vesicle, likewise significant depletion in the number and motility of sperm. Given individually or combined butylparaben and triclosan, significantly decreased testosterone, luteinizing hormone, and follicle‐stimulating hormone levels. Individual treatment with tested compounds caused significant elevation in the E2 level, whereas combined treatment did not alter the E2 level. Testicular DNA damage was recorded in all treated groups. Moreover, the testicular malondialdehyde level was significantly elevated, along with a significant decrease in catalase enzyme activity in all treated groups. Superoxide dismutase enzyme activity was significantly decreased in the butylparaben‐treated group, increased in the triclosan‐treated group, and nonsignificantly changed the butylparaben‐triclosan‐treated group. The combined treatment produced an endocrine disturbance with a concomitant induction of testicular oxidative stress, which may represent a common mechanism of endocrine disruptor‐mediated dysfunction. [ABSTRACT FROM AUTHOR]

In the present study genotoxic effects after combined exposure of human breast cell lines (MCF-10A, MCF-7 and MDB-MB-231) to silver nanoparticles (AgNP, citrate stabilized, 15 and 45 nm by STEM, Ag15 and Ag45, respectively) with aluminium chloride, butylparaben, or di- n -butylphthalate were studied. In MCF-10A cells exposed for 24 h to Ag15 at the concentration of 23.5 μg/mL a statistically significant increase in DNA damage in comet assay (SSB) was observed. In the presence of the test chemicals the genotoxic effect was decreased to a level comparable to control values. In MCF-7 cells a significant increase in SSB level was observed after exposure to Ag15 at 16.3 μg/mL. The effect was also diminished in the presence of the three test chemicals. In MDA-MB-231 cells no significant increase in SSB was observed, however increased level of oxidative DNA damage (incubation with Fpg enzyme) was observed after exposure to combinations of both AgNP with aluminium chloride. No increase in micronuclei formation was observed in neither cell line after the single nor combined treatments. Our results point to a low risk of increased genotoxic effects of AgNP when used in combination with aluminium salts, butylparaben or di- n -butylphthalate in consumer products. [ABSTRACT FROM AUTHOR]

The title 1:1 co-crystal, C11H14O3·C6H6N2O [systematic name: butyl 4-hydroxybenzoate–isonicotinamide (1/1)], crystallizes with one molecule of butylparaben (BPN) and one molecule of isonicotinamide (ISN) in the asymmetric unit. In the crystal, BPN and ISN molecules form hydrogen-bonded (O—H...N and N—H...O) dimers of paired BPN and ISN molecules. These dimers are further connected to each other via N—H...O=C hydrogen bonds, creating ribbons in [011] which further stack along the a axis to form a layered structure with short C...C contacts of 3.285 (3) Å. Packing interactions within the crystal structure were assessed using PIXEL calculations.

Gamma radiolysis and ozonolysis are two competitive advanced oxidation processes for degradation of organic pollutants present in the ground water. In this paper, the gamma radiolytic degradation of an emerging organic pollutant Butylparaben (BP) in aqueous solution has been investigated for the first time at different absorbed doses. The effect of the absorbed dose rate in the degradation and mineralization of BP has been investigated. About 65% mineralization of BP was observed at absorbed dose of 70 kGy and dose rate of 0.7 kGy h −1 . Interestingly, turbidity appeared in the solution during radiolysis at doses higher than 2 kGy, which disappeared again at very higher dose (~90 kGy) making the solution again transparent. At lower dose rate of 0.175 kGy h −1 the turbidity was appeared at much lower dose about 1 kGy. However, the dose rate showed no effect in the dose of the disappearance of the turbidity. The hydrophobic fragments insoluble in water were generated during the initial stage of gamma radiolysis and those were completely mineralized to CO 2 and H 2 O by direct absorption of gamma radiation. About 90 kGy dose was required to achieve ~90% mineralization of BP. On the contrary, maximum 50% mineralization was achieved after 5 h of ozonation at the O 3 flow rate of 0.5 L min −1 at pH 7.5 and it remained even constant upon prolonged ozonation. The oxygen-equivalent-chemical-oxidation-capacity (OCC) was used as the parameter to compare the % mineralization efficiencies of the two oxidative processes studied here and the gamma radiolysis was found to be more efficient between those processes. The phytotoxicity of the treated BP solution to agricultural seeds showed that the radiolytically generated fragments were less toxic compared to ozonolytically generated fragments. Thus gamma radiolysis is effective for reducing the organic burden and the toxicity of water polluted with emerging pollutants like BP. [ABSTRACT FROM AUTHOR]

The title 1:1 co-crystal, CnH11O3⋅C6H6N2O [systematic name: butyl 4-hydroxy-benzoate-isonicotinamide (1/1)], crystallizes with one molecule of butylparaben (BPN) and one molecule of isonicotinamide (ISN) in the asymmetric unit. In the crystal, BPN and ISN molecules form hydrogen-bonded (O--H ⋯ N and N -- H ⋯ O) dimers of paired BPN and ISN molecules. These dimers are further connected to each other via N--H ⋯ O=C hydrogen bonds, creating ribbons in [011] which further stack along the a axis to form a layered structure with short C⋯C contacts of 3.285 (3) Å. Packing interactions within the crystal structure were assessed using PIXEL calculations. [ABSTRACT FROM AUTHOR]