Aim:The aim was to evaluate the effect of multiple oral administration of bisphenol A (BPA) for 28 days on seminal characteristic on mammal using Wistar rat as a model.Materials and Methods:Rats were randomly divided into five different groups having 6 male rats in each group. The doses chosen were 50, 200, and 600 mg/kg body weight for Groups III, IV and V, respectively, based on preliminary dose range finding study and Group II served as vehicle control and Group I was negative control.Results:Reproductive study in the BPA-treated rats on day 28 revealed that there was significant (p≤0.05) reduction in the epididymal sperm count of rats of Group IV and significant (p≤0.01) decrease in Group V. Sperm motility percentage, dead count percentage, head and tail abnormality percentage were found to be significantly (p≤0.01) increased in rats of BPA-treated groups as compared to rats of control groups. Testes showed necrosis of germinal layer and spermatogonial cells in the seminiferous tubules. Hematological examination revealed significant (p≤0.01) decrease in the mean values of total erythrocyte count (TEC), total leukocyte count (TLC), hemoglobin, packed cell volume, and there was also significant (p≤0.05) lymphocytopenia in treated animals.Conclusion:It can be concluded from this study that subacute toxicity of BPA caused a reduction in the epididymal sperm count, sperm motility, dead count, head and tail abnormality, as well as hematological indices such as TLC, TEC etc. Hence, it appears that BPA affects the germ cells leading to impairment in the spermatogenesis, and thus having its property as reproductive toxicant and it also suppresses bone marrow functioning, which leads to normocytic hypochromic anemia in rats.

Over the past years, a growing body of work has linked numerous pervasive environmental chemicals with a multitude of adverse reproductive, developmental, behavioral, and metabolic changes in humans and animal models. Plasticizers include a wide variety of phthalate esters that are extensively used in a host of personal day care and cosmetic products. Many population-based studies have indicated a close association between diethyl phthalate (DEP) and diabetes albeit the mechanisms remain much unexplored. Presently, we report that long-term dietary administration of DEP to adult male Swiss albino mice at two different concentrations mirroring the recommended tolerable doses, severely impaired insulin signaling in hepatocytes and adipocytes. This was concomitant with sustained oxidative stress from the overactivation of NADPH oxidase 2, a major intracellular source of reactive oxygen species, in both the cell types. The present study provides evidences of the onset of insulin resistance in mice after chronic exposure to DEP in diet even at lower levels. This, in turn, can have serious pathological consequences with ultimate manifestations of type 2 diabetes and metabolic syndrome (MetS). Thus, by disrupting the central metabolic function of liver and adipose tissue, the key insulin target tissues, daily exposure to phthalates in plastics can potentially contribute to the alarming prevalence of MetS in recent times.

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The global burden of male infertility is rising at an alarming rate affecting the lives of millions in terms of physical, emotional and societal perspectives. Among several existing endocrine disrupting chemicals, bisphenol A (BPA) has been reported by many to inflict male reproductive toxicity in different experimental models, especially in mice. This review article critically discusses the overall reproductive toxicity of BPA with a special note to its ubiquitous existence, contamination route, effects on the reproductive system and toxicity mechanisms in male mice. Disturbed redox status in germ cells and spermatozoa plays a pivotal role in BPA induced male reproductive toxicity. In this context, the involvement of mitochondria and endoplasmic reticulum is also of grave importance. Induction of caspase-dependent apoptosis is the extreme consequence that leads to deterioration of cellular parameters. Besides the oxidative cellular and histoarchitectural damages, perturbed endocrine regulation, subsequent impaired hormonal and cellular genesis program, epigenetic alterations and inflammation cumulatively reflect poor sperm quality leading to compromised reproduction. Moreover, several key issues have also been highlighted that, if addressed, will strengthen our understanding of BPA mediated male reproductive toxicity.

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