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Aquat Toxicol. 2003 May 8;63(3):229-41.

Oxidative stress and loss of cortisol secretion in adrenocortical cells of rainbow trout (Oncorhynchus mykiss) exposed in vitro to endosulfan, an organochlorine pesticide.

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  • 1Département des Sciences Biologiques, Université du Québec à Montréal, TOXEN Research Centre, CP 8888, succ Centre-ville, Montréal, Qué, Canada H3C 3P8.


The effects of endosulfan, a widely used organochlorine pesticide, on cortisol secretion, cell viability, antioxidants and lipid peroxidation were investigated in enzymatically dispersed head kidney cells of rainbow trout (Oncorhynchus mykiss). ACTH- and dbcAMP-stimulated cortisol secretion, and cell viability were impaired in a dose-related manner following acute in vitro exposure to endosulfan (EC(50) 19 microM, LC(50) 366 microM) and the loss of cortisol secretion was detected even at concentrations of endosulfan that did not decrease cell viability. Stimulation with dbcAMP did not restore cortisol secretion in endosulfan exposed cells while stimulation with pregnenolone maintained cortisol secretion until viability of cells was affected. Thus endosulfan may disrupt processes between the step generating cAMP and the step where pregnenolone is used. Activity of catalase increased at concentrations of endosulfan that did not impair cortisol secretion, and decreased at higher doses. Glutathione peroxidase (GPx) activity was significantly reduced at doses of endosulfan that also reduced levels of glutathione, an essential cofactor of GPx. Exposure up to 1 x 10(-7) M endosulfan increased the activity of glutathione transferase. The present in vitro study identified endosulfan as a chemical inducing a loss of secretory responses in teleost adrenocortical steroidogenic cells and alterations in the activity of enzymes known to be involved in oxidative stress pathways. Moreover, the significant increase in lipid hydroperoxides levels provided further evidence for endosulfan-induced oxidative stress.

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