Perinatal Glutathione Levels in Liver and Brain of Rats from Large and Small Litters

For quantitative evaluation of lipid peroxidation after perinatal hypoxia in umbilical arterial cord blood samples from 109 healthy, acidotic, and asphyctic neonates with a gestational age ranging from 26 to 41 wk, the levels of aldehydic lipid peroxidation products malondialdehyde (MDA) and 4-hydroxynon-2-enal (HNE) were measured. Furthermore, the concentrations of oxidized and reduced glutathione (GSSH and GSH) and the purine compounds hypoxanthine and uric acid were determined. With increasing gestational age MDA and HNE levels increased. Furthermore, an increased level of GSH was also found. After perinatal hypoxia the concentrations of MDA and HNE rose distinctly (p < 0.001), reflecting sensitively the extent of in vivo lipid peroxidation. HNE is proposed to be a new parameter for quantitative evaluation of posthypoxic cellular damage in the perinatal period. HNE is a more specific parameter for estimation of lipid peroxidation processes in comparison with MDA. Additionally, HNE is cytotoxic and mutagenic at nanomolar concentrations. The increased levels of both MDA and HNE were accompanied by a strong decrease of GSH concentrations (p < 0.001), indicating the rapid consumption of GSH via a glutathione peroxidase reaction but additionally the high reactivity of HNE with sulfhydryl groups. During oxygen deficiency, increased levels of hypoxanthine (p < 0.01) and uric acid (p < 0.05) were due to the accelerated degradation of purine nucleotides. The rate of purine degradation including xanthine oxidase reactions characterizes the extent of an important radical source during oxygen deficiency, contributing to peroxidation of polyunsaturated fatty acids and the formation of peroxidation of polyunsaturated fatty acids and the formation of secondary aldehydic lipid peroxidation products.

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Aging, Training and Exercise

Kretzschmar

Müller

1993

Sports Medicine

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Changes in plasma glutathione (reduced form: GSH; oxidised form: GSSG) and lipid peroxides (LPO) levels occur with aging, training and acute physical exercise. Sources of plasma GSH, GSSG and LPO include the liver and skeletal muscle. Aging appears to be accelerated because of a decrease in the antioxidant capacity of tissues reflected in a decreased plasma GSH level. This age-dependent change could be partly compensated by physical training. Skeletal muscle appears to be able to deliver GSH into circulation with the adaptation of muscle to exercise training reflected in an increased plasma GSH level in the trained subject. Decreased plasma GSH concentration following physical exercise demonstrates increased GSH consumption in skeletal muscle resulting in a reduced export rate from muscle into plasma. The GSH system is able to effectively protect tissues against lipid peroxidation initiated by oxygen-derived free radicals produced in the intermediate metabolism during exercise. It can be assumed that the rate of this free radical production is a function of oxygen flow through organ and muscle tissue.

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Perinatal Glutathione Levels in Liver and Brain of Rats from Large and Small Litters

Cited by 3 publications

References 15 publications

Relationship between liver gamma-glutamyltranspeptidase activity and glutathione content in chronic-malnourished pups of adolescent rats

Relationship between liver gamma-glutamyltranspeptidase activity and glutathione content in chronic-malnourished pups of adolescent rats

Increased Levels of Lipid Peroxidation Products Malondialdehyde and 4-Hydroxynonenal after Perinatal Hypoxia

Aging, Training and Exercise

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