Why the study?
The role of PM2.5 on ischemia-reperfusion-associated mitochondrial dysfunction at the mitochondrial subpopulation level was not established.
Does PM2.5 administration exacerbate mitochondrial dysfunction in isolated rat hearts subjected to ischemia-reperfusion injury?
Does PM2.5 administration exacerbate mitochondrial dysfunction in isolated rat hearts subjected to ischemia-reperfusion injury?
Direct administration of PM2.5 to isolated rat hearts exacerbates ischemia-reperfusion injury by causing severe mitochondrial damage, particularly in the inter-fibrillar mitochondrial fraction.
Hypothesis-generating for PM2.5 effects on cardiac mitochondria in I/R; human studies required before clinical relevance.
A previous study has reported that exposure to PM2.5 from diesel exhaust (diesel particulate matter (DPM)) for 21 days can deteriorate the cardiac recovery from myocardial ischemia reperfusion injury (IR), where the latter is facilitated by the efficiency of mitochondrial subpopulations. Many investigators have demonstrated that IR impact on cardiac mitochondrial subpopulations is distinct. In the present study, we decipher the role of PM2.5 on IR associated mitochondrial dysfunction at the subpopulation level by administrating PM2.5 directly to isolated female rat hearts via KH buffer. Our results demonstrated that PM2.5 administered heart (PM_C) severely deteriorated ETC enzyme activity (NQR, SQR, QCR, and COX) and ATP level in both IFM and SSM from the normal control. Comparatively, the declined activity was prominent in IFM fraction. Moreover, in the presence of IR (PM_IR), mitochondrial oxidative stress was higher in both subpopulations from the normal, where the IFM fraction of mitochondria experienced elevated oxidative stress than SSM. Furthermore, we assessed the in vitro protein translation capacity of IFM and SSM and found a declined ability in both subpopulations where the inability of IFM was significant in both PM_C and PM_IR groups. In support of these results, the expression of mitochondrial genes involved in fission, fusion, and mitophagy events along with the DNA maintenance genes such as GUF1, LRPPRC, and HSD17-b10 were significantly altered from the control. Based on the above results, we conclude that PM2.5 administration to the heart inflicted mitochondrial damage especially to the IFM fraction, that not only deteriorated the cardiac physiology but also reduced its ability to resist IR injury.
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Sivakumar et al. (2022) studied this question.
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