Reperfusion Top Open Access Journals
The
reperfusion phase is taken into account a serious contributor of ROS. employing a global cerebral ischemia/reperfusion
model in gerbils, Cao et al. observed that
ischemia alone results in a marginal increase in ROS, while
ischemia and
reperfusion together cause massive increase in ROS. ROS were quantified by measuring conversion of salicylate, a comparatively non-toxic but highly effective hydroxyl trap. An identical study by Piantadosi and Zhang during a rat
model of worldwide cerebral
ischemia also confirmed production of ROS during post-ischemia reperfusion. However, ROS production was restored when rotenone was delivered along side succinate (substrate for mitochondrial electron transport chain complex II). This study suggests that complex I of the mitochondrial electron transport chain may be a major source of ROS during ischemia/reperfusion. The abrupt availability of oxygen during
reperfusion to highly reduced mitochondrial electron transport chain components and accumulated free electrons is believed to induce the discharge of
free radicals during post-ischemia reperfusion. Post-ischemia
reperfusion induces overload of the cellular
antioxidant defense capacity, leading to the depletion of all endogenous antioxidants, which inhibits
cells from restoring
antioxidant concentrations and results in exacerbated oxidative stress.
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