Physiological adaptation to chronic exposure to high fat diet and environmental pollutant (DDE) in rat testis

Fat intake induces metabolic disorders associated to obesity. Moreover, a wide range of hydrophobic chemicals, arrive to the body with contaminated foods acting as endocrine disruptors. Examples are represented by the organochlorine (OC)s at which belongs Dichlorodiphenildichloroethylene (DDE). These chemicals undergo to biomagnification producing oxidative stress, metabolic and hormonal disorders in mammalian. Our work was carried out to evaluate the adaptive responses in adult rat testis to which has administrated a non-toxic dose of DDE (10mg/Kg b.w.), for 28 days, alone or associated to high fat diet (HFD). 4 animal groups were used: N (Normal diet); D (HFD); D+DDE and N+DDE. Morphology of tubules was detected by using H&E stain. Lipid peroxidation, antioxidant activity and serum testosterone levels were measured with specific kits. Western blot analyses were done to test BAX, PCNA and androgen receptor (AR) protein levels. Finally, apoptotic cells were stained with caspase 3 immunohistochemistry. The results showed, in D group, increased lipid peroxidation, reduced antioxidant capacity, reduction of testosterone and AR levels, cellular damages and apoptosis. These results were found much more evident in DDE-treated groups, where the highest tissue damages occurred. In opposition to the rised negative effects, cellular proliferation increases in all groups, particularly in N+DDE. In conclusion, we assume that HFD and DDE produce cellular stress lead to antioxidant impairment, hormonal alteration, testicular damages and apoptosis more evident in presence of the pesticide. The increased cellular proliferation could be used to counterbalance the damages occurred following treatments, maintaining a pool of tubules that follow a physiological differentiation and maturation