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Protective effect of lycopene on adriamycin-induced cardiotoxicity and nephrotoxicity
Seval Yilmaz1, Ahmet Atessahin, Engin Sahna
1Department of Biochemistry, College of Veterinary Medicine, Faculty of Veterinary, Firat (Euphrates) University, 23119 Elazig, Turkey. sevyilars@yahoo.com
Abstract:
The aim of this study was to investigate the possible protective role of lycopene on adriamycin (ADR)-induced heart and kidney toxicity using biochemical and histopathological approaches. Rats were randomly divided into four groups. The first group received no medication and was regarded as the control group; the second group was injected with a single dose of ADR; the third group was treated with lycopene for 10 days before ADR injection and the last group was treated with lycopene for 2 days before and for 3 days after the administration of a single dose of ADR. ADR (10mg/kg) was intraperitoneally (i.p.) injected as a single dose and lycopene (4 mg/kg) was administered in corn oil by gavage. The levels of malondialdehyde (MDA) and reduced glutathione (GSH) in both the heart and kidneys were higher in the group treated with ADR alone than in the control group, and were lower in the groups administered with lycopene than in the ADR alone group. Although the activity of catalase (CAT) in the heart was higher in the ADR alone group than in the control group, it was lower in the kidneys. In particular, treatment with lycopene post-injection normalized both cardiac and kidney CAT activities. In heart and kidney tissues, glutathione peroxidase (GSH-Px) activities were not significantly different between all groups. Significant increases in the levels of plasma creatinine and urea were observed in the ADR group when compared to the control group, and these increases were normalized by lycopene treatment. Cardiac and renal histopathological changes were observed in the ADR group as compared to the control group. In contrast, these histopathological changes appeared nearly normal in the groups treated with lycopene pre- and post-injection. In conclusion, this study clearly indicated that ADR treatment markedly impaired cardiac and renal function and that treatment with lycopene might prevent this toxicity in rats.
Insights
Lycopene may protect against adriamycin (ADR) toxicity in the heart and kidneys. This study found lycopene treatment reduced biochemical and histopathological damage caused by ADR in rats.
Area of Science:
- Cardiovascular Science
- Nephrology
- Toxicology
Background:
- Adriamycin (ADR) is a potent chemotherapy agent with known cardiotoxic and nephrotoxic side effects.
- Oxidative stress plays a significant role in ADR-induced organ damage.
- Lycopene, a powerful antioxidant, has shown potential in mitigating various forms of toxicity.
Purpose of the Study:
- To evaluate the protective effects of lycopene against adriamycin-induced cardiotoxicity and nephrotoxicity in a rat model.
- To assess the impact of lycopene administration before and after ADR exposure on organ function and integrity.
Main Methods:
- Rats were divided into control, ADR-only, lycopene pre-treatment, and lycopene pre- and post-treatment groups.
- Biochemical markers including malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), plasma creatinine, and urea were measured.
- Histopathological examination of cardiac and renal tissues was performed.
Main Results:
- ADR administration significantly increased MDA and decreased GSH levels in heart and kidney tissues.
- ADR elevated plasma creatinine and urea levels, indicating impaired renal function.
- Histopathological analysis revealed significant cardiac and renal damage in ADR-treated rats, which was ameliorated by lycopene.
- Lycopene treatment normalized CAT activity in kidneys and partially in the heart, and reduced oxidative stress markers.
Conclusions:
- Adriamycin (ADR) significantly impairs cardiac and renal function.
- Lycopene demonstrates a protective role against ADR-induced cardiotoxicity and nephrotoxicity.
- Pre- and post-treatment with lycopene effectively mitigates ADR-induced organ damage in rats.
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