Acidosis-induced zinc-dependent death of cultured cerebellar granule neuronsстатья
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Дата последнего поиска статьи во внешних источниках: 18 июля 2013 г.
Аннотация:Severe acidosis caused death of cultured cerebellar granule neurons (CGNs).
Acidosis was accompanied by a progressive increase of the intracellular zinc ions
([Zn(2+)](i)) and decrease of [Ca(2+)](i). Zn(2+) chelator,
N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), prevented the increase
of [Zn(2+)](i) and acidosis-induced neuronal death. However, neuronal death was
insensitive to blockade of ASIC1 channels with amiloride, as CGNs display
considerably lower expression of ASIC1a than other neurons. The antioxidant
trolox and menadione significantly protected neurons from acidotic death.
Earlier, we demonstrated that menadione rescues neurons from the deleterious
effect of inhibition of mitochondrial complex I (Isaev et al. Neuroreport
15:2227-2231, 2004). We speculate that excessive Zn(2+)-dependent production of
reactive oxygen species by mitochondrial complex I may be a general motive for
the induction of cell death in CGNs under acidotic conditions.