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Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection.

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.

SUBMITTER: Plotnikov EY

PROVIDER: S-EPMC3746855 | biostudies-other | 2013 Aug

REPOSITORIES: biostudies-other

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Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection.

Plotnikov Egor Y EY Morosanova Maria A MA Pevzner Irina B IB Zorova Ljubava D LD Manskikh Vasily N VN Pulkova Natalya V NV Galkina Svetlana I SI Skulachev Vladimir P VP Zorov Dmitry B DB

Proceedings of the National Academy of Sciences of the United States of America 20130729 33

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 ...[more]

PMID: 23898194

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Project description:BackgroundMechanical ventilation is a life-saving intervention used to provide adequate pulmonary ventilation in patients suffering from respiratory failure. However, prolonged mechanical ventilation is associated with significant diaphragmatic weakness resulting from both myofiber atrophy and contractile dysfunction. Although several signaling pathways contribute to diaphragm weakness during mechanical ventilation, it is established that oxidative stress is required for diaphragmatic weakness to occur. Therefore, identifying the site(s) of mechanical ventilation- induced reactive oxygen species production in the diaphragm is important.ObjectiveThese experiments tested the hypothesis that elevated mitochondrial reactive oxygen species emission is required for mechanical ventilation-induced oxidative stress, atrophy, and contractile dysfunction in the diaphragm.DesignCause and effect was determined by preventing mechanical ventilation-induced mitochondrial reactive oxygen species emission in the diaphragm of rats using a novel mitochondria-targeted antioxidant (SS-31).InterventionsNone.Measurements and main resultsCompared to mechanically ventilated animals treated with saline, animals treated with SS-31 were protected against mechanical ventilation-induced mitochondrial dysfunction, oxidative stress, and protease activation in the diaphragm. Importantly, treatment of animals with the mitochondrial antioxidant also protected the diaphragm against mechanical ventilation-induced myofiber atrophy and contractile dysfunction.ConclusionsThese results reveal that prevention of mechanical ventilation-induced increases in diaphragmatic mitochondrial reactive oxygen species emission protects the diaphragm from mechanical ventilation-induced diaphragmatic weakness. This important new finding indicates that mitochondria are a primary source of reactive oxygen species production in the diaphragm during prolonged mechanical ventilation. These results could lead to the development of a therapeutic intervention to impede mechanical ventilation-induced diaphragmatic weakness.

Project description:ObjectiveTo study the effect of Antioxidants supplementation in reducing oxidative stress induced in acute amitriptyline poisoning cases.Design and methodsWe compared the effect of supplementation of treatment of acute amitriptyline poisoning cases with alpha lipoic acid alone or with vitamin C, with that of those receiving only routine standard treatment (RST) as a control group.A total of 132 subjects divided into 5 groups were selected from IMCU (Intensive Medical Care Unit) and Toxicology Ward, Govt. General Hospital, Chennai, India. The study was restricted to grade 1 coma in poisoned subjects per the Edinburg scale. Each of the subjects was in the groups were supplemented with either placebo, RST, RST with vitamin C, RST with ALA, or RST with vitamin C and ALA.Acute anti-depressant poisoning (especially with amitriptyline) induced oxidative stress caused lipid peroxidation. Plasma cholinesterases (chE) play a major role in combating this effect. A determination of the level of cholinesterase (chE) acts as an indirect indicator of the level of oxidative stress and a measure of the efficacy of antioxidant supplementation. Plasma cholinesterase estimation was done by colorimetric method. The change in color of the indicator bromothymol blue caused by the liberated acetic acid from cholinesterase read by spectrophotometer at 620 nm was used to determine the levels of cholinesterase.ResultA decrease in the level of oxidative stress was observed among those supplemented with either alpha lipoic acid alone or along with vitamin C, with a slightly more decrease in oxidative stress in the latter group. A p-value of <0.001 is considered significant statistically. The percentage of the benefit of treatment on supplementation with vitamin C and alpha lipoic acid showed a marked increase in group V (26.9%) cases after supplementation with both in combination.ConclusionThe results provide evidence that the oxidative stress induced by acute amitriptyline poisoning is comparatively decreased by supplementation with antioxidants like alpha lipoic acid and vitamin C, than those only on routine standard treatment.

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Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection.

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Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection.

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