Disrupted brain mitochondrial morphology after in vivo hydrogen sulfide exposure

被引:1
|
作者
Rumbeiha, Wilson K. [1 ]
Kim, Dong-Suk [1 ]
Min, Angela [1 ]
Nair, Maya [1 ]
Giulivi, Cecilia [1 ,2 ]
机构
[1] Univ Calif Davis, Sch Vet Med, Dept Mol Biosci, Davis, CA 95616 USA
[2] Univ Calif Davis, Med Invest Neurodev Disorders MIND Inst UCDH, Sacramento, CA 95616 USA
关键词
NICOTINAMIDE NUCLEOTIDE TRANSHYDROGENASE; NEUROLOGICAL SEQUELAE; EXERCISING MEN; RAT-BRAIN; INHALATION; LUNG; CELLS; DEGRADATION; MECHANISM; CRISTAE;
D O I
10.1038/s41598-023-44807-y
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Changes in mitochondrial dynamics are often associated with dietary patterns, medical treatments, xenobiotics, and diseases. Toxic exposures to hydrogen sulfide (H2S) harm mitochondria by inhibiting Complex IV and via other mechanisms. However, changes in mitochondrial dynamics, including morphology following acute exposure to H2S, are not yet fully understood. This study followed mitochondrial morphology changes over time after a single acute LCt50 dose of H2S by examining electron microscopy thalami images of surviving mice. Our findings revealed that within the initial 48 h after H2S exposure, mitochondrial morphology was impaired by H2S, supported by the disruption and scarcity of the cristae, which are required to enhance the surface area for ATP production. At the 72-h mark point, a spectrum of morphological cellular changes was observed, and the disordered mitochondrial network, accompanied by the probable disruption of mitophagy, was tied to changes in mitochondrial shape. In summary, this study sheds light on how acute exposure to high levels of H2S triggers alterations in mitochondrial shape and structure as early as 24 h that become more evident at 72 h post-exposure. These findings underscore the impact of H2S on mitochondrial function and overall cellular health.
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页数:14
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