SOURCE:

Faculty: Biosences
Department: Applied Biochemistry

CONTRIBUTORS:

Oguazu, C.E;
Ezeonu, F.C;

ABSTRACT:

Bisphenol A (BPA) is a monomer found in commonly used consumer plastic goods. Although much attention in recent years has been placed on BPA's impact as an endocrine disruptor, it also activates many immune pathways involved in both immune disease development and immune reactivity provocation. The current scientific literature has some research papers linking BPA directly to human or animal onset of immunity disorder, and despite reports indicating harmful effects of BPA, little is known about its role in oxidative stress responses. This research project explores the impact of BPA on, not only interleukins profile, but also the potential effects that BPA may have on the development or provocation of thyroid and sex hormone mechanisms, alongside oxidative stress and inflammation, using automated analyzer and ready to use kits. In this study, LD50, body weight and the effect of BPA exposure (0.05-1, mg/kg/BW) on an female wistar albino rats for 13 weeks by monitoring expression of biomarkers for sex hormone, thyroid hormones, gluthation system, endogenous antioxidants, thioredoxin system, peroxiredoxin system, lipid peroxidation, inflammation, and interleukin. In general, the LD50 obtained was above 2000mg/kg, dose dependent gain in body weight was observed at the onset of the experiment, which later decreased and the entire BPA exposure groups showed altered expression of all the biomarkers assayed. The results showed that BPA exposure at all the exposure doses, imposed oxidative stress on the rats and longer exposure time involved responses of immune-related conditions. BPA down-regulated the levels of some of the parameters assessed such as catalase, glutathione and superoxide dismutase for all the exposure-times while thioredoxine reductase, estrial, and follicle stimulating hormone were down-regulated after exposure. The up-regulation of interleukins was observed in most instances, while as the duration of the experiment increases, the concentrations of interleukins increased several fold compared to the control. This indicates the possible role of BPA-associated oxidative stress in induction of inflammatory response. Potential mechanisms by which BPA may be a contributing risk factor to immune disease development and progression include its impact on hormone; the thyroid and sex hormones, which include hyperprolactinemia, estrogenic signaling and hypothyroidism, triggering synthesis of more thyroid hormone. On the other hand BPA elicits oxidative stress on the cell and tissues of the animal by causing distortion of the antioxidant enzyme system; such as the endogenous antioxidant enzymes and the pereoxiredoxin system, glutathione system and thioredoxin system disruption, increased lipid peroxidation was also observed. With regards to inflammation biomakers, BPA could also be a contributing risk factor in the inflammatory signal transduction pathway alteration, immune signal transduction pathway alteration, cytokine activation. In this research project, it may be concluded that BPA trigger mechanisms that has a role in the pathogenesis of certain diseases conditions such as infertility, arthritis, and eventual celluler damage.