Melatonin ameliorates bisphenol A-induced biochemical toxicity in testicular mitochondria of mouse

Anjum, Sameya; Rahman, Shakilur; Kaur, Manpreet; Ahmad, Firoz; Rashid, Hina; Ansari, Rizwan; Raisuddin, Sheikh

doi:10.1016/j.fct.2011.07.062

Cited by 121 publications

(94 citation statements)

References 48 publications

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“…Consistent with studies before 2007 (Chitra et al 2003; Kabuto et al 2003, 2004), recent studies have shown that continuous exposure to low-dose BPA exposure induces DNA breaks and the production of ROS in mice and rats (Anjum et al 2011; Dobrzynska and Radzikowska 2013; Fang et al 2013; Liu et al 2013; Minamiyama et al 2010; Rashid et al 2009; Wu et al 2013) (see Supplemental Material, Table S7). Tiwari and Vanage (2013) reported that oral exposure to low-dose BPA for 6 days also induced sperm DNA damage.…”

Section: Sperm Production and Qualitysupporting

confidence: 78%

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Peretz

Vrooman

Ricke

et al. 2014

Environ Health Perspect

477

301

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Background: In 2007, an expert panel reviewed associations between bisphenol A (BPA) exposure and reproductive health outcomes. Since then, new studies have been conducted on the impact of BPA on reproduction.Objective: In this review, we summarize data obtained since 2007, focusing on a) findings from human and animal studies, b) the effects of BPA on a variety of reproductive end points, and c) mechanisms of BPA action.Methods: We reviewed the literature published from 2007 to 2013 using a PubMed search based on keywords related to BPA and male and female reproduction.Discussion: Because BPA has been reported to affect the onset of meiosis in both animal and in vitro models, interfere with germ cell nest breakdown in animal models, accelerate follicle transition in several animal species, alter steroidogenesis in multiple animal models and women, and reduce oocyte quality in animal models and women undergoing in vitro fertilization (IVF), we consider it an ovarian toxicant. In addition, strong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial proliferation, decreased uterine receptivity, and increased implantation failure in animal models. BPA exposure may be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired implantation in humans, but additional studies are required to confirm these associations. Studies also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, the placenta, and pubertal development.Conclusion: Based on reports that BPA impacts female reproduction and has the potential to affect male reproductive systems in humans and animals, we conclude that BPA is a reproductive toxicant.Citation: Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. 2014. Bisphenol A and reproductive health: update of experimental and human evidence, 2007–2013. Environ Health Perspect 122:775–786; http://dx.doi.org/10.1289/ehp.1307728

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Section: Sperm Production and Qualitysupporting

confidence: 78%

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Peretz

Vrooman

Ricke

et al. 2014

Environ Health Perspect

477

301

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“…Reduced glutathione (GSH) is the major nonprotein thiol and plays a pivotal role in cell viability protecting cells against lipid peroxidation either alone or in conjugation with other proteins (Anjum et al, 2011). In our study, we found a significant decrease in the amount of reduced GSH in liver and kidney of C.,idella exposed to sublethal concentration of BPA.…”

Section: Discussionsupporting

confidence: 55%

Oxidative stress and histopathologic biomarkers of exposure to bisphenol-A in the freshwater fish, Ctenopharyngodon idella

Faheem

Lone

2018

Braz. J. Pharm. Sci.

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Bisphenol-A (BPA) belongs to the family of endocrine disrupting chemicals (EDCs) and it is used in the production of polycarbonate plastic and epoxy resins. The reproductive toxicity of BPA is well documented but it also exerts its toxic effects through multiple pathways especially by inducing a state of oxidative stress and causing damage to the vital organs. In the present study, histopathologic and oxidative damage caused by BPA in liver and kidneys of fresh water cyprinid, Ctenopharyngodon idella was evaluated. LC 50 of BPA for Ctenopharyngodon idella was determined by probit regression analysis. Fish were exposed to a sublethal concentration of BPA i.e. 3.2 ppm (1/2 LC 50 ) for 14 days. Histologic studies revealed that BPA caused degenerative changes in liver and kidneys and exposure of sublethal concentration of BPA caused oxidative damage in both organs. Lipid peroxidation significantly increased in liver and kidneys of treated group. Catalase activity and reduced glutathione content significantly decreased in the group exposed to BPA compared to control and glutathione-S-transferase activity increased significantly in both organs exposed to the sublethal concentration of BPA. From this study it is concluded that BPA caused toxic effects in fish species by changing oxidative balance and damaging the vital organs.

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“…Isocitrate dehydrogenase 1 (IDH1) decarboxylates isocitrate to aketoglutarate (a-KG), leading to generation of NADPH, which is the reduced form of nicotinamide adenine dinucleotide phosphate, which is required to regenerate reduced glutathione (GSH), the major cellular ROS scavenger. A downregulation of this mitochondrial enzyme was shown in rat testis after cyclophosphamide treatment (Selvakumar et al, 2005) and in mouse testis after bisphenol-A treatment (Anjum et al, 2011).…”

mentioning

confidence: 98%

In Utero Exposure to Environmentally Relevant Concentrations of PCB 153 and PCB 118 Disrupts Fetal Testis Development in Sheep

Krogenæs

Ropstad

Gutleb

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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Polychlorinated biphenyls (PCB) are environmental pollutants linked to adverse health effects including endocrine disruption and disturbance of reproductive development. This study aimed to determine whether exposure of pregnant sheep to three different mixtures of PCB 153 and PCB 118 affected fetal testis development. Ewes were treated by oral gavage from mating until euthanasia (d 134), producing three groups of fetuses with distinct adipose tissue PCB levels: high PCB 153/low PCB 118 (n = 13), high PCB 118/low PCB 153 (n = 14), and low PCB 153/low PCB 118 (n = 14). Fetal testes and blood samples were collected for investigation of testosterone, testis morphology, and testis proteome. The body weight of the offspring was lower in the high PCB compared to the low PCB group, but there were no significant differences in testis weight between groups when corrected for body weight. PCB exposure did not markedly affect circulating testosterone. There were no significant differences between groups in number of seminiferous tubules, Sertoli cell only tubules, and ratio between relative areas of seminiferous tubules and interstitium. Two-dimensional (2D) gel-based proteomics was used to screen for proteomic alterations in the high exposed groups relative to low PCB 153/low PCB 118 group. Twenty-six significantly altered spots were identified by liquid chromatography (LC)-mass spectroscopy (MS)/MS. Changes in protein regulation affected cellular processes as stress response, protein synthesis, and cytoskeleton regulation. The study demonstrates that in utero exposure to different environmental relevant PCB mixtures exerted subtle effects on developing fetal testis proteome but did not significantly disturb testis morphology and testosterone production.

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Melatonin ameliorates bisphenol A-induced biochemical toxicity in testicular mitochondria of mouse

Cited by 121 publications

References 48 publications

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Oxidative stress and histopathologic biomarkers of exposure to bisphenol-A in the freshwater fish, Ctenopharyngodon idella

In Utero Exposure to Environmentally Relevant Concentrations of PCB 153 and PCB 118 Disrupts Fetal Testis Development in Sheep

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