Abstract
The writers showed previously that endogenous products of lipid peroxidation (LPO) accumulate in the liver in acute ischemia, and this correlates with depression of microsomal mono-oxygenase activity; it has been postulated that LPO processes participate in ischemic damage to NADPH-dependent oxygenases of the endoplasmic reticulum (ER) [5, 6]. It has also been shown that antioxidants inhibit accumulation of LPO products in ischemia and reoxygenation of different organs [i, 3, 9, i0] and that inducers of microsomal mono-oxygenases are responsible for preservation of a higher concentration of cytochrome P-450 and of the rate of N-demethylation of amidopyrine (AP) in ischemia of the liver [12].
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