Search

Background: Increasing evidence suggests that bisphenol A (BPA) induces liver pathological changes. Further, an association between BPA and circulating vitamin D (VitD) levels were documented. Aim: The role of VitD in BPA-induced liver pathological changes was explored in this study. Methods: Healthy 4.5-week-old male (n = 35) and female (n = 35) Swiss albino mice were used in this study. The animals were randomly divided into control and treated groups. The control groups were further divided into sham (no treatment) and vehicle (corn oil), whereas the treated groups were also divided into VitD (2195 U/kg), BPA (50 μg/kg), and BPA + VitD (50 μg/kg + 2195 U/kg) groups. For 6 weeks (twice a week), the animals were dosed intraperitoneally. One week later (at 10.5-weeks-old), the animals were sacrificed for biochemical and histological analyses. Results: BPA produced a considerable rise in the body and liver weights in both genders of mice when compared to control mice. BPA also caused significant increases in the liver damage markers alanine transaminase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT). It also induced liver histopathological changes, including higher apoptotic indices in both genders. On the other hand, treatment with VitD considerably reduced liver damage and slightly decreased the apoptotic index rate. The ALP, ALT, and GGT levels were also markedly reduced. VitD has been proven to have a protective effect on both genders. Conclusions: According to our findings, VitD protects mice from BPA-induced liver damage, possibly via suppressing liver damage markers. [ABSTRACT FROM AUTHOR]

Background: During early life, exposure to environmental toxicants, including endocrine disruptor bisphenol A (BPA), can be detrimental to the immune system. To our knowledge, a few researches have looked at the effects of developing BPA exposures on the spleen. Aim: The murine model was developed to investigate the underlying molecular mechanisms and mode of BPA actions on the spleen subsequent to prolonged early-life exposure to BPA. Methods: Immature (3-week-old) male and female Swiss Albino mice were intraperitoneally injected with 50 µg/kg BPA in corn oil or corn oil alone for 6 weeks. Mouse spleens were harvested and examined histologically at 10 weeks old (adulthood). Results: We observed neurobehavioral impairments and a significant increase in peripheral monocyte and lymphocyte counts in mice (males and females). Moreover, several spleen abnormalities in both male and female mice were observed in adulthood. BPA-treated mice's histopathological results revealed toxicity in the form of significantly active germinal centers of the white pulp and a few apoptotic cells. There was also a notable invasion of the red pulp by eosinophils and lymphocytes that were significantly higher than normal. Agarose gel electrophoresis provided further evidence of internucleosomal DNA fragmentation and apoptosis in the splenic tissues of BPA-treated mice compared to controls. In addition, there were increased levels of the lipid peroxidation malondialdehyde end-product, a marker of oxidative lipid damage, in the spleens of BPA-treated mice compared to controls. Conclusion: Our study provides evidence that oxidative stress injury induced by early-life exposures to BPA could contribute to a range of splenic tissue damages during adulthood. [ABSTRACT FROM AUTHOR]

Background: During early development, environmental compounds can induce adult onset diseases and disrupt the circulating vitamin D (VitD) levels. Aim: This study aimed to examine the protective role of VitD against the adverse effects of BPA on male and female mice. Methods: A total of 60 male and female Swiss Albino mice (3 weeks old) were randomly divided into 5 groups; each consisted of 12 mice (6 males and 6 females) and was treated as follows: Group I received no treatment (sham control); Group II, sterile corn oil only (vehicle control); Group III, BPA (400 μg/kg); Group IV, VitD (2,195 IU/kg); and Group V, BPA + VitD. At 10.5 weeks, the animals were sacrificed to conduct histological examinations. Results: BPA-exposed mice were found to have neurobehavioral abnormalities, heart, kidney, and lung diseases with increased apoptotic indices in both sexes. On the other hand, the treatment of BPA mice with VitD altered this scenario with modulated motor activity, enhanced body and organ weights, and preserved the heart, kidney, and lung architecture, alongside a decreased percent apoptotic index. Conclusion: Our findings illustrate that VitD protects mice against BPA-induced heart, kidney, and lung abnormalities. [ABSTRACT FROM AUTHOR]