Changes in mitochondrial and microsomal lipid peroxidation and fatty acid profiles in adrenal glands, testes, and livers from α-tocopherol-deficient rats

Studies were done to evaluate the effects of alpha -tocopherol deficiency in rats on the fatty acid composition and sensitivity to lipid peroxidation (LP) of mitochondria and microsomes from adrenal glands, testes, and livers. In control (alpha -tocophcrol-sufficient) animals, adrenal concentrations of alpha -tocopherol were approximately 10 times greater than those in livers and testes. Dietary deficiency of alpha -tocopherol for 8 weeks decreased adrenal and hepatic concentrations by 80-90% and testicular concentrations by approximately 60-70%. Incubation of testicular or hepatic mitochondria and microsomes from control rats with FeSO4 (1.0 mM) caused a time-dependent stimulation of LP as indicated by the formation of thiobarbituric acid reactive substances (TBARS); the rate of TEARS production increased in preparations from alpha -tocopherol-deficient animals. TEARS formation was not demonstrable in adrenal mitochondria or microsomes from alpha -tocopherol sufficient rats, but reached high levels in alpha -tocopherol-deficient preparations. The fatty acid composition of mitochondria and microsomes was tissue-dependent. In particular, arachidonio acid comprised approximately 40% of the total fatty acids in adrenal membranes, but only 20-25% in testes and livers, alpha -Tocopherol deficiency increased oleic acid concentrations in adrenal and hepatic mitochondria and microsomes but not in testes. In all three tissues, linoleic acid concentrations decreased by approximately 50%, but arachidonic acid levels were unaffected by alpha -tocopherol deficiency. The results indicate a close relationship between tissue sensitivity to LP in vitro and alpha -tocopherol concentrations. Nonetheless, any oxidative stress in vivo caused by alpha -tocopherol deficiency seems to spare arachidonic acid in mitochondria and microsomes but decreases linoleic acid concentrations. It is possible that because of the important physiological functions of arachidonic acid, metabolic adaptations serve to maintain membrane content during periods of oxidative stress. (C) 2001 Elsevier Science Inc.