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Oxidative damage and stress response from ochratoxin a exposure in rats
J C Gautier1, D Holzhaeuser, J Markovic
1Nestlé Research Center, Nestec Ltd., Lausanne, Switzerland.
Abstract:
Ochratoxin A (OTA) is a mycotoxin found in some cereal and grain products. It is a potent renal carcinogen in male rats, although its mode of carcinogenic action is not known. Oxidative stress may play a role in OTA-induced toxicity and carcinogenicity. In this study, we measured several chemical and biological markers that are associated with oxidative stress response to determine if this process is involved in OTA-mediated toxicity in rats. Treatment of male rats with OTA (up to 2 mg/ 24 h exposure) did not increase the formation of biomarkers of oxidative damage such as the lipid peroxidation marker malondialdehyde in rat plasma, kidney, and liver, or the DNA damage marker 8-oxo-7,8-dihydro-2' deoxyguanosine in kidney DNA. However, OTA treatment (1 mg/kg) did result in a 22% decrease in alpha-tocopherol plasma levels and a 5-fold increase in the expression of the oxidative stress responsive protein haem oxygenase-1, specifically in the kidney. The selective alteration of these latter two markers indicates that OTA does evoke oxidative stress, which may contribute at least in part to OTA renal toxicity and carcinogenicity in rats during long-term exposure.
Insights
Ochratoxin A (OTA) causes oxidative stress in rat kidneys, indicated by decreased alpha-tocopherol and increased haem oxygenase-1. This suggests oxidative stress may contribute to OTA
Area of Science:
- Toxicology
- Carcinogenesis
- Biochemistry
Background:
- Ochratoxin A (OTA) is a mycotoxin found in cereals.
- OTA is a known renal carcinogen in male rats.
- The mechanism of OTA carcinogenicity is not fully understood, but oxidative stress is implicated.
Purpose of the Study:
- To investigate the role of oxidative stress in Ochratoxin A-induced renal toxicity and carcinogenicity in male rats.
- To measure biomarkers of oxidative damage and oxidative stress response following OTA exposure.
Main Methods:
- Male rats were treated with varying doses of Ochratoxin A (OTA).
- Biomarkers of oxidative damage, including malondialdehyde and 8-oxo-7,8-dihydro-2' deoxyguanosine, were measured in plasma, kidney, and liver.
- Plasma alpha-tocopherol levels and kidney haem oxygenase-1 expression were assessed as indicators of oxidative stress response.
Main Results:
- OTA exposure did not increase biomarkers of direct oxidative damage (malondialdehyde, 8-oxo-7,8-dihydro-2' deoxyguanosine).
- OTA treatment significantly decreased plasma alpha-tocopherol levels by 22%.
- OTA significantly increased kidney haem oxygenase-1 expression by 5-fold, indicating an oxidative stress response.
Conclusions:
- Ochratoxin A exposure selectively alters markers associated with oxidative stress, specifically in the kidney.
- These findings suggest that OTA-induced oxidative stress plays a role in its renal toxicity and potential carcinogenicity in rats.
- Further research is warranted to elucidate the long-term effects and precise mechanisms of OTA-induced renal damage.
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