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DNA damage and the effect of antioxidants in streptozotocin-treated mice
1Safety Research Laboratory, Tanabe Seiyaku Co., Ltd, 3-16-89 Kashima, Yodogawa-ku, Osaka 532-8505, Japan. a-ima@tanabe.co.jp
Abstract:
Streptozotocin (STZ) has drawn attention as a potential source of oxidative stress, which induces genotoxicity. We investigated the effects of STZ on DNA damage in the liver and kidney, as well as the protective effects of antioxidants, by using the alkaline single-cell gel electrophoresis assay, and by measuring the ratio of 8-hydroxy-2'-deoxyguanosine (8-OHdG) to dG. A single intraperitoneal injection of STZ (150 mg/kg) increased serum levels of glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and blood urea nitrogen (BUN), and also caused DNA damage in the liver and kidney, which recovered slowly with time. Antioxidants,(ascorbic acid, trolox and probucol) prevented the STZ-induced elevation of DNA damage in the liver and kidney and inhibited the increase in serum levels of AST, ALT and BUN. Thus ascorbic acid, trolox, and probucol protected the mice against STZ-induced DNA damage that might contribute to the development of hepatic or renal disease.
Insights
Streptozotocin (STZ) induces DNA damage in liver and kidney cells, causing oxidative stress. Antioxidants like ascorbic acid, trolox, and probucol effectively protected against this STZ-induced genotoxicity and related organ damage.
Area of Science:
- Biochemistry
- Toxicology
- Genetics
Background:
- Streptozotocin (STZ) is recognized for inducing oxidative stress and genotoxicity.
- Oxidative stress is implicated in DNA damage within vital organs.
Purpose of the Study:
- To investigate STZ's effects on DNA damage in the liver and kidney.
- To evaluate the protective potential of antioxidants against STZ-induced genotoxicity.
Main Methods:
- Utilized the alkaline single-cell gel electrophoresis assay to detect DNA damage.
- Measured the ratio of 8-hydroxy-2'-deoxyguanosine (8-OHdG) to deoxyguanosine (dG).
- Assessed serum levels of glucose, AST, ALT, and BUN.
Main Results:
- STZ administration (150 mg/kg) significantly increased DNA damage in liver and kidney tissues.
- STZ elevated serum markers of liver and kidney injury (AST, ALT, BUN).
- Antioxidants (ascorbic acid, trolox, probucol) mitigated STZ-induced DNA damage and biomarker increases.
Conclusions:
- Ascorbic acid, trolox, and probucol demonstrate protective effects against STZ-induced DNA damage.
- These antioxidants may prevent hepatic and renal diseases associated with STZ exposure.
- Findings highlight the role of antioxidants in combating STZ-related oxidative stress and genotoxicity.
