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Simulated microgravity-induced mitochondrial dysfunction in rat cerebral arteries.

Ran Zhang1, Hai-Hong Ran2, Li-Li Cai3

  • 1Institute of Geriatric Cardiology.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|March 8, 2014
PubMed
Summary

Simulated microgravity causes mitochondrial dysfunction in rat brain arteries, increasing oxidative stress. This cerebrovascular damage involves NADPH oxidase and mitochondria crosstalk, impacting cardiovascular health.

Keywords:
NADPH oxidasehindlimb unweightingoxidative stress

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Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Space Medicine

Background:

  • Spaceflight-induced microgravity leads to cardiovascular deconditioning.
  • Cerebrovascular oxidative stress injury is a potential consequence of microgravity exposure.
  • Mitochondrial dysfunction may underlie cerebrovascular changes during simulated microgravity.

Purpose of the Study:

  • To investigate if simulated microgravity induces mitochondrial dysfunction in rat arteries.
  • To elucidate the mechanisms of cerebrovascular injury under simulated microgravity conditions.

Main Methods:

  • Hindlimb unweighting (HU) was used to simulate microgravity in rats for four weeks.
  • Mitochondrial function markers (ROS, Δψm, mPTP, RCR, antioxidant enzymes, MDA) were assessed in cerebral and mesenteric VSMCs.
  • The effects of apocynin (NADPH oxidase inhibitor) and mitoTempol (antioxidant) were evaluated.

Main Results:

  • Simulated microgravity significantly increased mitochondrial ROS, mPTP opening, and MDA in cerebral arteries.
  • Δψm, RCR, and antioxidant enzyme activity/expression decreased in cerebral arteries but not mesenteric arteries.
  • Apocynin and mitoTempol treatments partially restored mitochondrial function in HU rat cerebral arteries.

Conclusions:

  • Simulated microgravity induces cerebrovascular mitochondrial dysfunction.
  • Crosstalk between NADPH oxidase and mitochondria plays a role in this process.
  • These findings highlight potential mechanisms for cardiovascular changes in space.