Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury
A previous study has reported that exposure to PM<sub>2.5</sub> 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 subp...
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MDPI AG
2022-12-01
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author | Bhavana Sivakumar Abdullah F. AlAsmari Nemat Ali Mohammad Waseem Gino A. Kurian |
author_facet | Bhavana Sivakumar Abdullah F. AlAsmari Nemat Ali Mohammad Waseem Gino A. Kurian |
author_sort | Bhavana Sivakumar |
collection | DOAJ |
description | A previous study has reported that exposure to PM<sub>2.5</sub> 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 PM<sub>2.5</sub> on IR associated mitochondrial dysfunction at the subpopulation level by administrating PM<sub>2.5</sub> directly to isolated female rat hearts via KH buffer. Our results demonstrated that PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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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spelling | doaj.art-b5331edf55d548809f4bf1adffc9db332023-11-24T13:23:54ZengMDPI AGBiology2079-77372022-12-011112181110.3390/biology11121811Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion InjuryBhavana Sivakumar0Abdullah F. AlAsmari1Nemat Ali2Mohammad Waseem3Gino A. Kurian4Vascular Biology Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thanjavur 613401, Tamil Nadu, IndiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Maryland Eastern Shore, Princess Anne, MD 21853, USAVascular Biology Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thanjavur 613401, Tamil Nadu, IndiaA previous study has reported that exposure to PM<sub>2.5</sub> 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 PM<sub>2.5</sub> on IR associated mitochondrial dysfunction at the subpopulation level by administrating PM<sub>2.5</sub> directly to isolated female rat hearts via KH buffer. Our results demonstrated that PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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.https://www.mdpi.com/2079-7737/11/12/1811particulate matterinter-fibrillar mitochondriadiesel exhaustischemia reperfusion injurycardiomyocytes |
spellingShingle | Bhavana Sivakumar Abdullah F. AlAsmari Nemat Ali Mohammad Waseem Gino A. Kurian Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury Biology particulate matter inter-fibrillar mitochondria diesel exhaust ischemia reperfusion injury cardiomyocytes |
title | Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury |
title_full | Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury |
title_fullStr | Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury |
title_full_unstemmed | Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury |
title_short | Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury |
title_sort | consequential impact of particulate matter linked inter fibrillar mitochondrial dysfunction in rat myocardium subjected to ischemia reperfusion injury |
topic | particulate matter inter-fibrillar mitochondria diesel exhaust ischemia reperfusion injury cardiomyocytes |
url | https://www.mdpi.com/2079-7737/11/12/1811 |
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