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Glutathione Deficiency Leads to Mitochondrial Damage in Brain
Ajey Jain, Johannes Martensson, Einar Stole, Peter A. M. Auld, and Alton
Meister
Proc. Nati. Acad. Sci. USA Vol. 88, pp. 1913-1917, March 1991.
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ABSTRACT
Glutathione deficiency induced
in newborn rats by giving buthionine sulfoximine, a selective inhibitor of
y-glutamylcysteine synthetase, led to markedly decreased cerebral cortex
glutathione levels and striking enlargement and degeneration of the
mitochondria. These effects were prevented by giving glutathione monoethyl
ester, which relieved the glutathione deficiency, but such effects were
not prevented by giving glutathione, indicating that glutathione is not
appreciably taken up by the cerebral cortex. Some of the oxygen used by
mitochondria is known to be converted to hydrogen peroxide. We suggest
that in glutathione deficiency, hydrogen peroxide accumulates and damages
mitochondria. Glutathione, thus, has an essential function in mitochondria
under normal physiological conditions. Observations on turnover and
utilization of brain glutathione in newborn, preweaning, and adult rats
show that (i) some glutathione turns over rapidly (t˝,
≈30 min in adults, ≈8
min in newborns), (ii) several pools of glutathione probably exist, and
(iii) brain utilizes plasma glutathione, probably by y-glutamyl
transpeptidase-initiated pathways that account for some, but not all, of
the turnover; thus, there is recovery or transport of cysteine moieties.
These studies provide an animal model for the human diseases involving
glutathione deficiency and are relevant to oxidative phenomena that occur
in the newborn.
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