Acute high-altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

急性高原缺氧暴露通过甲醛积累导致神经功能障碍

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作者:Xiaoyin Wang, Haochen Sun, Lili Cui, Xian Wang, Changhong Ren, Zhiqian Tong, Xunming Ji

Aims

In this study, we aimed to investigate whether cerebral FA was accumulated after hypobaric hypoxia exposure, and further explored the preventative effect of CoQ10 through FA elimination.

Conclusion

Cerebral FA accumulation mediates neurological deficits under acute hypobaric hypoxia, and CoQ10 supplementation may be a promising preventative strategy for visitors and sojourners at plateau.

Results

Accumulated cerebral FA was found in C57BL/6 mice after acute high-altitude hypoxia exposure, which resulted in FA metabolic disturbance with the elevation of semicarbazide-sensitive amine oxidase, and declination of aldehyde dehydrogenase-2. Excessive FA was also found to induce neuronal ferroptosis in vivo. Excitingly, administration with CoQ10 for 3 days before acute hypobaric hypoxia reduced cerebral FA accumulation, alleviated subsequent neuronal ferroptosis, and preserved neurological functions.

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