Next Article in Journal
Impact of Intravenous Iron on Oxidative Stress and Mitochondrial Function in Experimental Chronic Kidney Disease
Previous Article in Journal
Neuroprotection after Hemorrhagic Stroke Depends on Cerebral Heme Oxygenase-1
Open AccessArticle

N-Acetylcysteine Attenuates the Increasing Severity of Distant Organ Liver Dysfunction after Acute Kidney Injury in Rats Exposed to Bisphenol A

1
Renal Physiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
2
Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand
3
Cardiac Electrophysiology Research and Training Center, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
*
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(10), 497; https://doi.org/10.3390/antiox8100497
Received: 12 September 2019 / Revised: 11 October 2019 / Accepted: 17 October 2019 / Published: 21 October 2019
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
Distant organ liver damage after acute kidney injury (AKI) remains a serious clinical setting with high mortality. This undesirable outcome may be due to some hidden factors that can intensify the consequences of AKI. Exposure to bisphenol A (BPA), a universal chemical used in plastics industry, is currently unavoidable and can be harmful to the liver. This study explored whether BPA exposure could be a causative factor that increase severity of remote liver injury after AKI and examined the preventive benefit by N-acetylcysteine (NAC) in this complex condition. Male Wistar rats were given vehicle, BPA, or BPA + NAC for 5 weeks then underwent 45 min renal ischemia followed by 24 h reperfusion (RIR), a group of vehicle-sham-control was also included. RIR not only induced AKI but produced liver injury, triggered systemic oxidative stress as well as inflammation, which increasing severity upon exposure to BPA. Given NAC to BPA-exposed rats diminished the added-on effects of BPA on liver functional impairment, oxidative stress, inflammation, and apoptosis caused by AKI. NAC also mitigated the abnormalities in mitochondrial functions, dynamics, mitophagy, and ultrastructure of the liver by improving the mitochondrial homeostasis regulatory signaling AMPK-PGC-1α-SIRT3. The study demonstrates that NAC is an effective adjunct for preserving mitochondrial homeostasis and reducing remote effects of AKI in environments where BPA exposure is vulnerable. View Full-Text
Keywords: acute kidney injury; bisphenol A; ischemia and reperfusion; liver; mitochondria; N-acetylcysteine; oxidative stress; remote organ injury acute kidney injury; bisphenol A; ischemia and reperfusion; liver; mitochondria; N-acetylcysteine; oxidative stress; remote organ injury
Show Figures

Figure 1

MDPI and ACS Style

Peerapanyasut, W.; Kobroob, A.; Palee, S.; Chattipakorn, N.; Wongmekiat, O. N-Acetylcysteine Attenuates the Increasing Severity of Distant Organ Liver Dysfunction after Acute Kidney Injury in Rats Exposed to Bisphenol A. Antioxidants 2019, 8, 497.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop