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<p>Deep metabolic transitions promoted by anoxia and diapause are tolerated for years by embryos of the brine shrimp, <i>Artemia franciscana</i>, whereas even short metabolic disruptions in mammals are accompanied by bursts of reactive oxygen species (ROS) that cause tissue damage during ischemia–reperfusion. We hypothesized mitochondria from these embryos are mechanistically poised to avoid ROS bursts and the associated oxidative stress during metabolic recovery. Isolated mitochondria that exhibited robust functional coupling were exposed to anoxia-reoxygenation (A/R) or continuous normoxia. H<sub>2</sub>O<sub>2</sub> efflux was statistically identical between A/R versus normoxia groups (p = 0.221). Addition of auranofin and dinitrochlorobenzene, inhibitors of ROS scavenging pathways, promoted a five-fold increase in H<sub>2</sub>O<sub>2</sub> release for the normoxic mitochondria, which confirmed that scavenging mechanisms substantially suppress routine ROS efflux. Yet when these same inhibitors were added to the A/R group, maximum H<sub>2</sub>O<sub>2</sub> efflux was no greater than for normoxia. Treatment with rotenone, an inhibitor of Complex I and reverse electron transport (RET), produced only a modest decrease in H<sub>2</sub>O<sub>2</sub> efflux. This result indicates that RET, a major contributor to ROS bursts in mammalian mitochondria, is not stimulated by A/R in <i>A. franciscana</i>. Lack of aconitase inactivation, protein carbonyl accumulation, and lipid hydroperoxide production demonstrate that bouts of A/R do not cause significant oxidative damage in <i>A. franciscana</i> mitochondria. Finally, the capacity to downregulate Complex I activity through active-deactive conformations was tested and is not operative. These data collectively suggest that Complex I from <i>A. franciscana</i> may not possess the capacity for RET and the associated ROS surge.</p>

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Low oxidative stress during mitochondrial recovery from anoxia in Artemia franciscana, an invertebrate extremophile

  • 期刊论文

  • 发表日期：

    2025年8月26日

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  • Daniel A. Arabie,
  • Olivia G. Moncrief,
  • Samantha M. Shirmer,
  • Steven C. Hand

摘要

Deep metabolic transitions promoted by anoxia and diapause are tolerated for years by embryos of the brine shrimp, Artemia franciscana, whereas even short metabolic disruptions in mammals are accompanied by bursts of reactive oxygen species (ROS) that cause tissue damage during ischemia–reperfusion. We hypothesized mitochondria from these embryos are mechanistically poised to avoid ROS bursts and the associated oxidative stress during metabolic recovery. Isolated mitochondria that exhibited robust functional coupling were exposed to anoxia-reoxygenation (A/R) or continuous normoxia. H2O2 efflux was statistically identical between A/R versus normoxia groups (p = 0.221). Addition of auranofin and dinitrochlorobenzene, inhibitors of ROS scavenging pathways, promoted a five-fold increase in H2O2 release for the normoxic mitochondria, which confirmed that scavenging mechanisms substantially suppress routine ROS efflux. Yet when these same inhibitors were added to the A/R group, maximum H2O2 efflux was no greater than for normoxia. Treatment with rotenone, an inhibitor of Complex I and reverse electron transport (RET), produced only a modest decrease in H2O2 efflux. This result indicates that RET, a major contributor to ROS bursts in mammalian mitochondria, is not stimulated by A/R in A. franciscana. Lack of aconitase inactivation, protein carbonyl accumulation, and lipid hydroperoxide production demonstrate that bouts of A/R do not cause significant oxidative damage in A. franciscana mitochondria. Finally, the capacity to downregulate Complex I activity through active-deactive conformations was tested and is not operative. These data collectively suggest that Complex I from A. franciscana may not possess the capacity for RET and the associated ROS surge.