IS OXIDATIVE DAMAGE THE BIOCHEMICAL MECHANISM OF CELLULAR INJURY AND NECROSIS IN CHOLINE DEFICIENCY?

REPETTO, M.

Buenos Aires, Argentina.

Conferencia; Oxidative stress ans antioxidants; 2009

Faculatd de Farmacia y Bioquimica, UBA.

Oxidative stress and damage, determined as decreased tissue antioxidant levels, consumption of tissue alpha-tocopherol and increased lipid peroxidation, occur earlier than necrosis in weanling rats fed a choline deficient (CD) diet in liver, heart, kidney and brain. In the tissues, water soluble antioxidants were determined as total reactive antioxidant potential (TRAP), alpha-tocopherol content was estimated from homogenate chemiluminescence (homogenate-CL), and lipid peroxidation was determined as thiobarbituric acid reactive substances (TBARS). Histopathology showed hepatic steatosis at days 1-7, tubular and glomerular necrosis at days 6 and 7 in kidney, and inflammation and necrosis at days 6 and 7 in heart. TRAP levels decreased by 18%, 48%, 56% and 66% at day 7, with lifetimes for reach half maximal change of 2.0, 1.8, 2.5 and 3.0 days in liver, kidney, heart and brain, respectively. Homogenate-CL increased by 97%, 113%, 18% and 297% at day 7, with half lifetimes of 2.5, 2.6, 2.8 and 3.2 days in the four organs, respectively. TBARS contents increased by 98%, 157%, 104% and 347% at day 7, with half lifetimes of 2.6, 2.8, 3.0 and 5.0 days in the four organs, respectively. Plasma showed decrease of 33% in TRAP and a 5-times increase in TBARS at day 5. Oxidative stress and damage are processes earlier than necrosis in kidney and heart. There is no necrosis in liver where steatosis is previous to antioxidant consumption and increased lipid peroxidation.