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Activity and gene expression profile of certain antioxidant enzymes to microcystin-LR induced oxidative stress in
R Jayaraj1, T Anand, P V Lakshmana Rao
1Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Jhansi Road, Gwalior 474002, India.
Abstract:
Microcystins are cyclic heptapeptide toxins produced by certain strains of Microcystis aeruginosa and microcystin-LR (MC-LR) is the most toxic among the 70 variants isolated so far. These toxins have been implicated in both human and livestock mortality. In the present study we investigated the microcystin-LR induced oxidative stress in mice in terms of its effect on activity and gene expression profile of certain antioxidant enzymes and expression of heat shock protein-70 (HSP-70). Mice were treated with 0.5 LD50 (38.31 microg/kg) and 1 LD50 (76.62 microg/kg) and the biochemical variables were determined at 1, 3, 7 days and 15, 30, 60 and 120 min post-exposure for 0.5 and 1 LD50 dose, respectively. A significant time-dependent increase in HSP-70 expression over control was observed at 1 LD50 dose. The toxin induced significant increase in liver body weight index, hepatic lipid peroxidation and depletion of GSH levels at 1 LD50 compared to control group. There was significant decrease in the activity of antioxidant enzymes glutathione peroxidase (GPX), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-S-transferase (GST) at 1 LD50. Except catalase, there was no effect on other antioxidant enzymes at 0.5 LD50 dose. In contrast to activity of antioxidant enzymes the gene expression profile did not show any significant difference compared to control at 1 LD50. GR showed significant decrease in expression at 1, 3 and 7 days in animals dosed with 0.5 LD50 MC-LR. The results of our in vivo study clearly show the oxidative stress induced by MC-LR, and a correlation with activity and regulation at gene expression level of antioxidant enzymes.
Insights
Microcystin-LR (MC-LR) toxin causes oxidative stress in mice, decreasing antioxidant enzyme activity but not gene expression. This highlights MC-LR
Area of Science:
- Environmental Toxicology
- Biochemistry
- Molecular Biology
Background:
- Microcystins are potent cyclic heptapeptide toxins produced by Microcystis aeruginosa.
- Microcystin-LR (MC-LR) is the most toxic variant and linked to animal mortality.
- Oxidative stress is a key mechanism in toxin-induced cellular damage.
Purpose of the Study:
- To investigate MC-LR-induced oxidative stress in mice.
- To analyze the effects of MC-LR on antioxidant enzyme activity and gene expression.
- To examine the expression of heat shock protein-70 (HSP-70).
Main Methods:
- Mice were exposed to 0.5 and 1 LD50 doses of MC-LR.
- Biochemical variables, antioxidant enzyme activities, and gene expression were measured at various time points.
- Liver body weight index, hepatic lipid peroxidation, and glutathione (GSH) levels were assessed.
Main Results:
- A significant time-dependent increase in HSP-70 expression was observed at 1 LD50.
- MC-LR (1 LD50) increased liver body weight index, lipid peroxidation, and depleted GSH.
- Antioxidant enzyme activities (GPX, SOD, CAT, GR, GST) significantly decreased at 1 LD50, while gene expression showed no significant change.
- Glutathione reductase (GR) gene expression decreased at 0.5 LD50 MC-LR.
Conclusions:
- MC-LR induces significant oxidative stress in mice.
- MC-LR affects antioxidant enzyme activity more than gene expression.
- The findings correlate MC-LR exposure with oxidative stress and altered antioxidant enzyme regulation.
