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The protection of selenium on adriamycin-induced mitochondrial damage in rat
1Department of Physiology, Faculty of Medicine, University of Erciyes, Kayseri, Turkey.
Abstract:
Although adriamycin (ADR) exhibits high anti-tumor efficacy in vitro, its clinical use in cancer chemotherapy is limited due to its high renal toxicity. This study investigated the mechanism of ADR nephropathy and the protective effect of selenium on ADR-induced kidney damage by analyzing of the relationship between selenium and mitochondria. Rats were divided into four groups. The first group was injected with saline i.p. for 21 days, the second group received the 4 mg/kg i.p. ADR every alternate day for 8 days, the third group received the 50 μg/kg i.p. Se for 21 days, and the fourth group received the Se. ADR co-administration i.p. blood pressures were assessed, the mitochondrial membrane potential (MMP) was assessed, and the adenosine triphosphate (ATP) levels were determined. The total antioxidant (TAS) and oxidant status (TOS) in cytosol, the mitochondria of kidney cells, and plasma were measured. Mitochondrial TAS decreased and TOS increased in the ADR group compared to the Se group. ADR-treated rats showed significantly lower MMP than did the control and Se groups. MMP was significantly restored in the Se + ADR group through selenium treatment compared to the ADR group (p < 0.01). In the ADR group, a reduction in ATP content was seen compared to the control and Se groups (p < 0.01). ATP level was significantly restored through treatment with selenium in the Se + ADR group compared to the ADR group (p < 0.01). We concluded that selenium is effective in vivo against ADR-induced kidney damage via the restoration of TAS and TOS, which prevented mitochondrial damage.
Insights
Selenium protects against adriamycin (ADR)-induced kidney damage by restoring antioxidant balance and preventing mitochondrial dysfunction. This study highlights selenium
Area of Science:
- Nephrology
- Mitochondrial Biology
- Cancer Chemotherapy
Background:
- Adriamycin (ADR) is an effective anti-tumor drug but causes significant renal toxicity, limiting its clinical use.
- Understanding the mechanisms of ADR-induced nephropathy is crucial for developing protective strategies.
- Mitochondria play a key role in cellular damage and energy production, making them a focus in ADR toxicity research.
Purpose of the Study:
- To investigate the mechanism of adriamycin (ADR)-induced nephropathy.
- To evaluate the protective effect of selenium (Se) against ADR-induced kidney damage.
- To analyze the relationship between selenium and mitochondrial function in the context of ADR toxicity.
Main Methods:
- Rats were divided into four groups: control (saline), ADR-treated, selenium (Se)-treated, and Se + ADR co-treated.
- Measurements included blood pressure, mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) levels, and total antioxidant status (TAS) and oxidant status (TOS) in kidney cells and plasma.
- Mitochondrial function and oxidative stress markers were assessed.
Main Results:
- ADR treatment led to decreased mitochondrial TAS and increased TOS.
- ADR-induced rats exhibited significantly lower MMP and ATP levels compared to control and Se groups.
- Selenium treatment significantly restored MMP and ATP levels in the Se + ADR group compared to the ADR group (p < 0.01).
Conclusions:
- Selenium effectively protects against ADR-induced kidney damage in vivo.
- Selenium restores antioxidant balance (TAS/TOS) and prevents mitochondrial damage.
- Selenium's protective effect involves the restoration of mitochondrial membrane potential and ATP levels.
