For several decades, medicine has noted an increase in proliferative diseases, lipid overload and neurodegenerative diseases. The metabolic diseases are the most common (insulin resistance, type II diabetes or obesity disease). It is obvious that these diseases are multifactorial. An environmental cause is more and more frequently evoked as a causal factor or worsening factor. The last decades have seen a proliferation of the use of pesticides in agricultural or industrial uses. These xenobiotics are suspected to promote diseases called "environmental". It appears that even low doses of these products induce metabolic effects. We studied the effect of two organochlorine, lindane and chlordecone on mitochondrial function and cellular energy metabolism. This study was conducted on HepG2 cells, and short periods with concentrations corresponding to plasma concentrations found in the areas of exposure. These pesticide molecules induce mitochondrial stress that seems to resolve over a short period. However some disturbance of mitochondrial metabolic regulations and nucleo-mitochondrial cross-talk persist over longer periods. This is true for the expression of regulatory factors, disturbance promoting cellular dysfunction that may be the cause of "environmental" disease. We propose that the analysis of the mitochondrial function could be an interesting approach of low dose xénobiotics toxicological assesment.
