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Oxidative damage and gene expression profile of antioxidant enzymes after T-2 toxin exposure in mice
Manjari Chaudhari1, R Jayaraj, S R Santhosh
1Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Gwalior 474002, Madhya Pradesh, India.
Abstract:
T-2 toxin is one of the most potent trichothecenes, and on exposure causes severe human and animal diseases. We investigated the dose- and time-dependent effect of T-2 toxin on certain biochemical variables, oxidative damage in terms of antioxidant enzyme activity, and gene expression profile in mice. Mice treated intraperitoneally with either 1 LD50 or 2 LD50 dose (5.61 and 11.22 mg/kg body weight, respectively) of T-2 toxin showed significant alterations in hepatic alanine amino transferase, aspartate amino transferase, and lactate dehydrogenase. Significant changes in hepatic lipid peroxidation, depletion of glutathione (GSH), and expression of heat shock protein-70 indicated oxidative damage. We also evaluated the activity of antioxidant enzymes and compared the gene expression profile by quantitative real-time reverse transcriptase-polymerase chain reaction. Except for glutathione reductase (GR), there was a significant increase in activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase at 1 LD50 dose. At 2 LD50 dose, SOD showed decrease in activity, whereas GST, GPx, and catalase showed significant increase. In contrast, gene expression profile showed downregulation in GR, GPx, GST, and catalase at 1 LD50 dose. At 2 LD50 dose except GSH synthetase, all other genes were downregulated. The results clearly show oxidative stress as one of the mechanisms of T-2 toxin-mediated toxicity.
Insights
T-2 toxin exposure causes significant biochemical changes and oxidative stress in mice. This study reveals T-2 toxin-induced oxidative damage and altered antioxidant enzyme activity and gene expression.
Area of Science:
- Toxicology
- Biochemistry
- Molecular Biology
Background:
- T-2 toxin is a potent trichothecene mycotoxin causing severe health issues in humans and animals.
- Understanding its toxicological mechanisms is crucial for public health and animal safety.
Purpose of the Study:
- To investigate the dose- and time-dependent effects of T-2 toxin on biochemical variables in mice.
- To assess T-2 toxin-induced oxidative damage by evaluating antioxidant enzyme activity and gene expression profiles.
Main Methods:
- Mice were treated with 1 or 2 LD50 doses of T-2 toxin.
- Biochemical parameters (ALT, AST, LDH), lipid peroxidation, and glutathione levels were measured.
- Antioxidant enzyme activity and gene expression (quantitative real-time RT-PCR) were analyzed.
Main Results:
- T-2 toxin significantly altered hepatic enzymes (ALT, AST, LDH) and increased lipid peroxidation.
- Glutathione levels decreased, indicating oxidative stress.
- Antioxidant enzyme activity showed mixed responses, while gene expression generally downregulated, except for GSH synthetase at higher doses.
Conclusions:
- Oxidative stress is a key mechanism underlying T-2 toxin toxicity.
- T-2 toxin exposure leads to significant biochemical alterations and impacts antioxidant defense systems at both activity and gene expression levels.
