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Updated: May 9, 2026
Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection
Egor Y Plotnikov1, Maria A Morosanova, Irina B Pevzner
1A. N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow 119992, Russia.
Abstract:
Acute pyelonephritis is a potentially life-threatening infection of the upper urinary tract. Inflammatory response and the accompanying oxidative stress can contribute to kidney tissue damage, resulting in infection-induced intoxication that can become fatal in the absence of antibiotic therapy. Here, we show that pyelonephritis was associated with oxidative stress and renal cell death. Oxidative stress observed in pyelonephritic kidney was accompanied by a reduced level of mitochondrial B-cell lymphoma 2 (Bcl-2). Importantly, renal cell death and animal mortality were both alleviated by mitochondria-targeted antioxidant 10(6'-plastoquinonyl) decylrhodamine 19 (SkQR1). These findings suggest that pyelonephritis can be treated by reducing mitochondrial reactive oxygen species and thus by protecting mitochondrial integrity and lowering kidney damage.
Insights
Acute pyelonephritis causes oxidative stress and kidney damage. A novel antioxidant, SkQR1, protected kidney cells and reduced mortality in animal models, suggesting a new treatment approach for this severe infection.
Area of Science:
- Nephrology
- Infectious Diseases
- Mitochondrial Medicine
Background:
- Acute pyelonephritis is a severe upper urinary tract infection.
- Inflammation and oxidative stress in pyelonephritis lead to kidney damage and potential fatality.
- Mitochondrial dysfunction is implicated in the pathogenesis of kidney injury.
Purpose of the Study:
- To investigate the role of oxidative stress and mitochondrial B-cell lymphoma 2 (Bcl-2) in pyelonephritis-induced kidney damage.
- To evaluate the therapeutic potential of a mitochondria-targeted antioxidant in a pyelonephritis model.
Main Methods:
- Induction of pyelonephritis in an animal model.
- Assessment of oxidative stress markers and renal cell death.
- Measurement of mitochondrial Bcl-2 levels.
- Administration of the mitochondria-targeted antioxidant SkQR1.
Main Results:
- Pyelonephritis was confirmed to be associated with significant oxidative stress and renal cell death.
- Mitochondrial Bcl-2 levels were reduced in kidneys affected by pyelonephritis.
- Treatment with SkQR1 effectively alleviated renal cell death and reduced animal mortality.
Conclusions:
- Oxidative stress and mitochondrial dysfunction play a critical role in acute pyelonephritis.
- Targeting mitochondrial reactive oxygen species with antioxidants like SkQR1 offers a promising therapeutic strategy.
- Protecting mitochondrial integrity can mitigate kidney damage and improve outcomes in pyelonephritis.
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