Induction of oxidative stress by bisphenol A in the epididymal sperm of rats

Toxicology ◽  
2003 ◽  
Vol 185 (1-2) ◽  
pp. 119-127 ◽  
Author(s):  
K Chitra
Toxin Reviews ◽  
2021 ◽  
pp. 1-10
Author(s):  
Gulnaz Afzal ◽  
Hafiz Ishfaq Ahmad ◽  
Adil Jamal ◽  
Ghulam Mustafa ◽  
Shumaila Kiran ◽  
...  

Author(s):  
Alessandro Federico ◽  
Marcello Dallio ◽  
Antonietta Gerarda Gravina ◽  
Nadia Diano ◽  
Sonia Errico ◽  
...  

Introduction: Bisphenol A (BPA) exposure has been correlated to non-alcoholic fatty liver disease (NAFLD) development and progression. We investigated, in a clinical model, the effects of the administration of 303 mg of silybin phospholipids complex, 10 μg of vitamin D, and 15 mg of vitamin E (RealSIL, 100D, IBI-Lorenzini, Aprilia, Italy) in male NAFLD patients exposed to BPA on metabolic, hormonal, and oxidative stress-related parameters. Methods: We enrolled 32 male patients with histologic diagnosis of NAFLD and treated them with Realsil 100D twice a day for six months. We performed at baseline clinical, biochemical, and food consumption assessments as well as the evaluation of physical exercise, thiobarbituric acid reactive substances (TBARS), plasmatic and urinary BPA and estrogen levels. The results obtained were compared with those of healthy control subjects and, in the NAFLD group, between baseline and the end of treatment. Results: A direct proportionality between TBARS levels and BPA exposure was shown (p < 0.0001). The therapy determined a reduction of TBARS levels (p = 0.011), an improvement of alanine aminotransferase, aspartate aminotransferase, insulinemia, homeostatic model assessment insulin resistance, C reactive protein, tumor necrosis factor alpha (p < 0.05), an increase of conjugated BPA urine amount, and a reduction of its free form (p < 0.0001; p = 0.0002). Moreover, the therapy caused an increase of plasmatic levels of the native form of estrogens (p = 0.03). Conclusions: We highlighted the potential role of BPA in estrogen oxidation and oxidative stress in NAFLD patients. The use of Realsil 100D could contribute to fast BPA detoxification and to improve cellular antioxidant power, defending the integrity of biological estrogen-dependent pathways.


Chemosphere ◽  
2019 ◽  
Vol 234 ◽  
pp. 682-689 ◽  
Author(s):  
Jianqin Yuan ◽  
Yanbiao Kong ◽  
Mohammad Mehdi Ommati ◽  
Zhongwei Tang ◽  
Hong Li ◽  
...  

2016 ◽  
Vol 97 (5) ◽  
pp. 369-379 ◽  
Author(s):  
Sahar El-Sayed Elswefy ◽  
Fatma Rizk Abdallah ◽  
Hebatallah Husseini Atteia ◽  
Alaa Samir Wahba ◽  
Rehab Abdallah Hasan

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1201
Author(s):  
Claudio Pirozzi ◽  
Adriano Lama ◽  
Chiara Annunziata ◽  
Gina Cavaliere ◽  
Clara Ruiz-Fernandez ◽  
...  

Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA’s worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity.


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