Phospholipase A2 of rat liver mitochondria in vitamin E deficiency

Abstract

1. There is a more than 2-fold increase in phospholipase A(2) activity (EC 3.1.1.4) of liver mitochondria isolated from vitamin E-deficient rats compared with that in normal rats. 2. alpha-Tocopherol in lipoprotein-bound form is more effective than free alpha-tocopherol in restoring the enzyme activity to normal.

Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases

“…These changes include oxidative lesions in the mtDNA (Ames et al, 1993), oxidation of mitochondrial lipids, increased levels of long-chain polyunsaturated fatty acid, decreased membrane phospholipid peroxidability and decreased Δ9-desaturase activity coefficient leading to decreased levels of 16:1 and 18:1 fatty acids with less membrane stability. Additional mechanisms include increased apoptotic pathways, and increased inner mitochondrial phospholipase A 2 activity (Laganiere , Byung, 1993;Pappu et al, 1978). The content of cytochrome oxidase is associated with loss of enzymatic activity (Wilson , Franks, 1975), while malondialdehyde accumulation increases (Von Zglinicki et al, 1991).…”

“…Increased inner mitochondrial phospholipase A 2 activity (Laganiere and Byung, 1993) (Pappu et al, 1978) Content of cytochrome oxidase Loss of enzymatic activity (Wilson and Franks, 1975) Malondehaldeide accumulation Increase (Von Zglinicki et al, 1991) Mitochondrial number Decrease (Cogger et al, 2014;Gan et al, 2011;Premoli et al, 2009) Intracellular oxidant production (dichlorofuorescin)…”

Aging-like alterations of SDH activity in Purkinje cell mitochondria of adult vitamin-E deficient rats

“…The causative events responsible of these alterations appear to be shared by aging and vitamin E deficiency and may be singled out as the ubiquitous deterioration due to uncontrolled oxidative processes markedly occurring in both these conditions. An increased production of oxidants has been documented by the increased activity of phospholipase A 2 at the inner membranes of liver mitochondria of old (27) and adult vitamin Edeficient rats (28), thus strengthening the concept of the high risk of damage of these organelles to free radical attacks. With specific reference to SDH, the above assumption is supported by the wealth of current experimental data confirming that membrane functions are seriously compromised both in aging and vitamin E deficiency and this, in turn, may affect SDH specificity (29,30) as well as modify the enzyme's molecular structure (31).…”

Lysosomal membrane stabilization by α-tocopherol against the damaging action of Vipera russelli venom phospholipase A2

“…All other chemicals used were of analytical grade. Laboratory inbred Wistar strain albino rats of both sexes weighing 100 9 10 g were divided into three groups and maintained on a vitamin E-deficient diet [4] for (about) 4 months under the following conditions: 1) group A -no added vitamin E in diet 2) group B -100 mg of h-tocopherol acetate per kilogram of diet 3) group C -200 m of h-tocopherol acetate per kilogram of diet The onset of vitamin E deficiency was determined by the erythrocyte hemolysis test [5] and plasma tocopherol levels of rats. In order to investigate the effect of injected purified viper venom PLA 2 (VPR-PL-Vi) [6] on the lipid composition of the liver lysosomal membranes from different groups of rats, four to five animals from each group were given intraperitoneal injections of viper venom PLA 2 at a dose of 3.5 mg/g body weight and were killed at 5 h post injection.…”