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Prevention of cadmium‐induced effects on regional glutathione status of rat brain by vitamin E
Author(s) -
Shukla Girja S.,
Srivastava R. S.,
Chandra S. V.
Publication year - 1988
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550080504
Subject(s) - glutathione , chemistry , cadmium , glutathione reductase , endocrinology , medicine , vitamin e , vitamin , glutathione disulfide , antioxidant , biochemistry , enzyme , biology , glutathione peroxidase , organic chemistry
The effect of vitamin E on the cadmium‐induced changes of glutathione metabolism was investigated in different brain regions. Daily intraperitoneal injection of cadmium (0.4 mg/kg) for 30 days significantly decreased the concentration of reduced glutathione (GSH), and the activities of glutathione reductase (GR) and glucose‐6‐phosphate dehydrogenase (GPDH) in the cerebellum, cerebral hemispheres and brain stem of rats. Cadmium elevated the levels of oxidized glutathione (GSSG) in cerebellum and cerebral hemisphere regions only, while the GSH/GSSG ratio decreased in all three brain regions. The only effect of intramuscular injections of vitamin E (5 mg/kg) given on alternate days for 30 days was a slight increase in GSH and GR in the cerebral hemispheres. The simultaneous administration of vitamin E and cadmium prevented cadmium‐induced changes in GSH and GSSG levels and in the GSH/GSSG ratio, but the cerebellar GSH remained lowered. Furthermore, vitamin E, with the exception of GR in the cerebral hemispheres, did not prevent cadmium‐induced changes in enzyme activities. As the simultaneous injections of vitamin E reduced cadmium‐induced alterations in glutathione concentration without having any appreciable effect on the activity of related enzymes, it is suggested that the preventive effect of vitamin E is mediated through its antioxidative effect, saving GSH from oxidative destruction in the brain of cadmium‐exposed rats.