PUFA-restorative effect on the dimethoate induced damage on rat Leydig cell steroidogenesis

HURTADO DE CATALFO, GRACIELA; ASTIZ MARIANA; TACCONI DE ALANIZ M.J.; MARRA CARLOS ALBERTO

San Luis

Congreso; XLVII Reunión de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2011

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Previous studies from our lab demonstrated that dimethoate (D) administered to rats produce a strong inhibition of the androgenic activity in testis. The mechanism involves the inhibition of the StAR protein, stimulation of COX-2 and inhibition of steroidogenic enzymes (HSD) via ROS overproduction. In this work we studied the possible reversion of the damage by co-incubation of D with various fatty acids in isolated Leydig cells. The level of expression of StAR protein was increased by 20:4n-6 (AA) and, to a lesser extent, by 20:3n-6 (ETA), while 22:4n-6 (DTA), 22:6n-3 (DHA) and 22:5n-3 (DPA) did not show any effect. AA and ETA increased COX-2 expression and the production of PGF2a and E2, TBARS, the content of cholesterol and AA in mitochondrial phospholipids, while they decreased the activities of 3b and 17bHSD. DTA increased TBARS production and decreased both HSD activities. DHA and DPA strongly inhibited the expression of COX-2 and the production of PGs, the level of TBARS and the phospholipase A2 activity. Both acids increased mitochondrial cholesterol and the activities of HSD enzymes. As a result of the balance between these variables, the decreased production of testosterone caused by D treatment was restored by AA, DHA and DPA. DTA evidenced no restorative effect and DTA not only failed to restored but also caused an ulterior decrease of the androgen biosynthesis.