Oxidative stress and immune disturbance after long-term exposure to bisphenol A in juvenile common carp (Cyprinus carpio)

Qiu, Wenhui; Chen, Jingsi; Li, Yijie; Chen, Zhong; Jiang, Lihui; Yang, Ming; Wu, Minghong

doi:10.1016/j.ecoenv.2016.04.014

Cited by 80 publications

(28 citation statements)

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“…Eid, Eissa, and El‐Ghor () and Qiu et al. () reported the generation of increased oxidative stress and DNA damage by BPA exposure in rat and common carp respectively.…”

Section: Discussionmentioning

confidence: 99%

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Bisphenol A induced oxidative stress and apoptosis in mice testes: Modulation by selenium

2017

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Spermatogenesis, a highly coordinated process, is prone to environmental insults which may lead to impaired spermatogenesis or, at worst, infertility. Bisphenol A (BPA) is a well-known global environmental toxicant and a ubiquitous oestrogenic chemical. This study evaluated the role of selenium (0.5 ppm sodium selenite/kg diet) on spermatogenesis after BPA treatment in different groups of male BALB/c mice: control, selenium, BPA and selenium+BPA. Markers of oxidative stress and apoptosis were evaluated in testis after BPA treatment. Significant decrease in sperm concentration and motility and increased reactive oxygen species(ROS) and LPO levels were seen in BPA group. Histopathological changes revealed extensive vacuolisation, lumen devoid of spermatozoa and decreased germ cell count, confirmed by testicular germ cell count studies. TUNEL assay for apoptosis showed increased number of TUNEL-positive germ cells in BPA group with increased percentage apoptotic index. However, in Se+BPA group, histopathological studies revealed systematic array of all germ cells, preserved basement membrane with relatively less vacuolisation, improved sperm parameters and ROS and LPO levels and decreased number of TUNEL-positive germ cells. These results clearly demonstrate the role of selenium in ameliorating oxidative stress and apoptosis induced upon BPA treatment in mice and can be further used as therapeutic target in male infertility.

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“…Eid, Eissa, and El‐Ghor () and Qiu et al. () reported the generation of increased oxidative stress and DNA damage by BPA exposure in rat and common carp respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Qiu et al. () reported that high levels of BPA exposure result in increased generation of reactive oxygen species culminating in oxidative stress. Reports also suggest that BPA exposure is associated with spermatogenic cell apoptosis (Takahashi & Oishi, ).…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A induced oxidative stress and apoptosis in mice testes: Modulation by selenium

2017

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“…Due to maternal-derived immune factors, lysozyme activity in fish embryos partly reflects maternal plasma activity. Although serum lysozyme activity in adult zebrafish was not assayed previous work suggests that low concentrations of BPA increase serum lysozyme activity in common carp (Cyprinus carpio) (Qiu et al, 2016a). For F1 larvae not exposed to bisphenol, slight or significant increases in lysozyme activity and gene expression were noted, indicating maternal transfer of increased lysozymes to offspring perhaps due to maternal induction after exposure.…”

Section: Discussionmentioning

confidence: 99%

Parental exposure to bisphenol A and its analogs influences zebrafish offspring immunity

Dong

Zhang

Meng

et al. 2018

Science of The Total Environment

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Transgenerational effects of environmental pollutants on humans and animals are complex. Thus, we used zebrafish to evaluate the effects of parental whole-life cycle exposure to bisphenol A and its analogs (bisphenol S and F) on offspring innate immunity. At adulthood, offspring were examined with/without continued chemicals treatment until 72h post-fertilization (hpf). To measure offspring immune function, larvae at 72 hpf were expose for 24h with/without the viral mimic polyinosinic-cytidylic acid (Poly I:C) or the bacterial mimic Pam3Cys-Ser-Lys4 (PAM3CSK4). Data show modified immunity in offspring. Specifically, lysozyme activity was significantly induced in F1 larvae and respiratory burst response and oxidative defense genes were inhibited. Genes of the innate immune system including Toll-like receptors and their downstream molecules and inflammatory cytokines were significantly down-regulated, whereas matrix metalloproteinases were up-regulated in larvae. In addition, recombination-activating genes in the immature adaptive immune system were significantly reduced. Thus, immune defense is diminished by exposing parental generations of zebrafish to environmentally relevant concentration of bisphenols and this suggests that fish chronically exposed to bisphenols in the wild may be vulnerable to pathogens.

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“…Oxidative stress describes the condition in which levels of oxygen and oxygen-derived free radicals overwhelm the natural antioxidant defenses naturally present in the cell and results in the damage of cellular components, inactivate essential metabolic enzymes and disrupt signal transduction pathways. Chemically, oxidative stress is associated with increased production of reactive oxidizing species (ROS) or a significant decrease in the effectiveness of antioxidant defenses 41,58,59 .…”

Section: Bpa Induced Oxidative Stress and Generation Of Rosmentioning

confidence: 99%

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2019

IJPSR

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Bisphenol-A (BPA), 2,2-bis(4-hydroxyphenyl) propane is an emerging environmental toxicant with endocrine disrupting properties and toxic effects on living organisms. BPA is ubiquitously present in consumer products current in our daily lives. As it is released from consumer products and deposited in the environment, thus creating the potential for human exposure through oral, inhaled, and dermal routes. BPA exposure might be able to cause oxidative damage by disturbing the balance between reactive oxygen species (ROS) and the antioxidant defense system of eukaryotic cells, resulting in the development of oxidative stress-related diseases. From the available information, it can be inferred that a wide variety of BPA intake through any mode results into a generation of reactive oxygen species (ROS), altering the antioxidant balance of eukaryotic cells, induces mitochondrial dysfunction, and affects cell signaling pathways related to oxidative stress. BPA induced oxidative stress might be able to cause sperm damage, mitochondrial dysfunction, and impairment of the structure and function of spermatozoa resulting in male infertility. Here, a review of the current literature examining literature related to BPA exposure, induction of ROS or oxidative stress and concludes that it alters reproductive system functions through induced oxidative stress pathways and negatively affects the fertility of male and females.

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Oxidative stress and immune disturbance after long-term exposure to bisphenol A in juvenile common carp (Cyprinus carpio)

Cited by 80 publications

References 50 publications

Bisphenol A induced oxidative stress and apoptosis in mice testes: Modulation by selenium

Bisphenol A induced oxidative stress and apoptosis in mice testes: Modulation by selenium

Parental exposure to bisphenol A and its analogs influences zebrafish offspring immunity

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