Effects of testosterone propionate (TP, 2.5 mg kg(-1) body weight) in fenvalerate-induced (120 mg kg(-1) body weight) thyroid dysfunction and lipid peroxidation were investigated in male mice. Testosterone propionate aggravated in the inhibition of hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, coupled with a decrease in serum triiodothyronine (T3) concentration in pesticide-treated mice. However, it could ameliorate the toxicity as indicated by decreased hepatic lipid peroxidation (LPO) with a marginal but significant increase in superoxide dismutase and catalase activities following fenvalerate treatment. While protective effects of testosterone on LPO indicated its antiperoxidative property, the decrease in 5'D-I activity could be because of the increased accumulation of fenvalerate in the tissues following TP administration.

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PubMedDate not supplied

Is triiodothyronine capable of ameliorating pyrethroid-induced thyroid dysfunction and lipid peroxidation?

A study on the effect of triiodothyronine (T3) in the regulation of pyrethroid (fenvalerate)-induced thyroid dysfunction and lipid peroxidation was carried out in male mice. Fenvalerate (120 mg kg(-1) body wt. daily for 15 days) administration led to a decrease in the serum concentration of thyroid hormones and the activity of hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) and an increase in the level of lipid peroxidation. The decrease in the activity of hepatic 5'D-I due to the administration of fenvalerate was restored with the administration of T3 (7 microg kg[-1] body wt. on alternate days). The increased level of lipid peroxidation was also ameliorated by T3. However, T3 could not restore the serum concentration of thyroxine (T4), only that of T3. We suggest that the ameliorating role of T3 in the fenvalerate-intoxicated mice could be the result of the lipogenic action of the thyroid hormone, which in turn led to the restoration of 5'D-I activity.

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PubMedDate not supplied

Possible involvement of lipid peroxidation in the inhibition of type I iodothyronine 5'-monodeiodinase activity by lead in chicken liver.

The possible involvement of lipid peroxidation (LPO) in the lead-induced inhibition of type I iodothyronine 5'-monodeiodinase activity (5'-D) has been worked out in chicken liver. Lead nitrate (1.5 mg per bird per day) for 30 days increased the lipid peroxidative process with a concomitant decrease in 5'-D activity in chicken liver. Also, a significant decrease in serum triiodothyronine (T3) concentration and an increase in serum thyroxine (T4) concentration were observed. The data suggest that lead-induced inhibition of type I 5'-D activity in chicken liver is mediated through the lipid peroxidative process.

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PubMedDate not supplied

Role of ascorbic acid in cadmium-induced thyroid dysfunction and lipid peroxidation.

A study on the effects of ascorbic acid (AA) on heavy metal (cadmium)-induced thyroid dysfunction and lipid peroxidation (LPO) was carried out in Swiss male mice. The animals were administered with either cadmium (1.0 mg kg(-1) body wt.) alone or in combination with AA (1 mM) every day for 15 days. While cadmium treatment led to a decrease in the serum concentrations of thyroid hormones and hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, an increase in the level of lipid peroxidation was observed. The metal-induced decrease in hepatic 5'D-I activity and serum triiodothyronine (T3) concentration was restored by treatment with AA. However, AA could not restore the serum thyroxine (T4) concentration. The increased level of LPO was also ameliorated by AA. It appears that the protective effect of AA against cadmium-induced thyroid dysfunction is mediated through its antioxidative action.

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