Physiological adaptations and tissue damage induced by a simultaneous chronic exposure to environmental pollutants and hyperlipidic diets: focus on mitochondrial and cellular stress in rat model.

Dichlorodipheniletylhene (DDE) is the main metabolite of dichlorodiphenilethane (DDT), a hydrophobic insecticide still used today in malaria world areas. These chemicals accumulate in fatty tissues arriving to human by consuming contaminated foods. The aim of work was the evaluation of low chronic oral exposure DDE (10mg/Kg b.w.) effects on mitochondrial function and tissue alteration in liver, kidney, testis, and brown adipose tissue (BAT) for 4 weeks, alone or in combination with a high fat diet (HFD, 45% fats) in the context of obesity. Tissues morphology was tested by using haematoxylin & eosin associated to immunostaining. Mitochondrial function was tested polarographically. The main proteins involved in cellular stress were analysed by western blot. Oxidative stress and antioxidant system activities were detected spectrophotometrically. In testis, DDE altered spermatogenesis inducing apoptosis, cell stress, and antioxidant system impairment. In liver and kidney, lipid accumulation, oxidative stress, and tissue alteration were found in both HFD and DDE groups. Interesting, antioxidant system was stimulated. Mitochondrial function was detected in testis, liver, and BAT evidencing organelles impairment. Moreover, BAT mitochondrial mass was found reduced by DDE. As a whole, our data show that both HFD and DDE can alter cellular function involving mitochondria and that physiological adaptative responses are activated to partially control tissues stress.