Time-dependent effects on body weight gain and hepatic oxidative stress in rats exposed to both high fat feeding and low doses of persistent organic pollutant

Background: Oxidative stress plays an important role into obesity associated metabolic comorbidities. Moreover, exposure to persistent organic pollutants (POPs) is associated with hepatic cellular stress due to detoxification processes. Little is known on the impact associated with chronic simultaneous exposure to both high-fat diet and low doses of persistent organic pollutants, such as p,p´-diphenyldichloroethene (DDE), (DDT’s major metabolite with the highest persistence). Aim: The present work aimed to investigate the effect of different periods of simultaneous exposure to low dose of POP and high-fat feeding on body weight gain and hepatic injury. Given that liver is the main organ involved in response to both high fat diet and toxic injury, we evaluated the development of oxidative stress at the hepatic level. Methods: Three groups of 8 rats were so treated for 4 or 16 weeks: 1) standard diet (10% fat J/J) (N rats); 2) high-fat diet (45% fat J/J) (D rats); 3) high-fat diet plus DDE (10 mg/kg b.w. by gavage) (D+DDE rats). DDE dose used in this work was comparable to the admissible daily intake. Body weight gain and hepatic lipid content were determined. Hepatic oxidative stress was assessed by determining H2O2 production and TBARs content. Results: D rats showed higher body weight gain, hepatic lipid content, H2O2 production and TBARs content compared to control rats after both 4 and 16 weeks. Similar variations were found in D+DDE rats after 4 weeks of treatment. On the other hand, after 16 weeks of treatment D+DDE rats showed lower body weight gain and hepatic lipid content compared to D rats. Moreover, they showed higher H2O2 production and TBARs content compared to D rats. Conclusion: Short period exposure to DDE associated with high fat feeding elicited the same alterations in body weight gain and hepatic oxidative stress found in response to the only exposure to high fat diet. A prolonged period of exposure revealed DDE treatment toxicity as showed by decreased body weight gain and hepatic lipid content and increased oxidative stress.