Effects of melatonin on lipid peroxidation and antioxidative enzyme activities in the liver, kidneys and brain of rats administered with benzo(a)pyrene

Dec 1, 2009Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie

Melatonin's effects on cell damage and antioxidant enzymes in the liver, kidneys, and brain of rats given benzo(a)pyrene

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Abstract

Melatonin co-administered with benzo(a)pyrene significantly reduced lipid peroxidation levels in brain, liver, and kidneys.

Lower levels of lipid peroxidation products were observed in all organs of rats treated with both B(a)P and melatonin compared to those treated with B(a)P only.
Following B(a)P administration, reduced glutathione levels decreased in the brain and kidneys.
Melatonin increased reduced glutathione levels in the liver and brain when co-administered with B(a)P.
The activity of superoxide dismutase increased in rats treated with melatonin, with the highest activity found in those treated with both B(a)P and melatonin.
Catalase activity was elevated in melatonin-treated rats and further increased in those receiving both B(a)P and melatonin across all tested tissues.

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Benzo(a)pyrene [B(a)P] is a widespread pollutant with a mutagenic, carcinogenic and strong prooxidative properties. The present study evaluated the melatonin effects on lipid peroxidation products levels and on activity of antioxidative enzymes in the course of B(a)P intoxication. Control rats were treated with 0.9% NaCl; another group was given 10mg melatonin/kg bw; a third group was injected twice a week with B(a)P at the dose of 10mg/kg bw; the fourth group received both B(a)P and melatonin at the dose as mentioned above. The experiment continued for 3 months. In homogenates of brain, liver and kidneys lipid peroxidation was appraised by evaluation of malonyldialdehyde and 4-hydroxyalkenal (MDA+4HDA) levels. Activities of glutathione peroxidase (GPx), superoxide dysmutase (SOD) and catalase (CAT) and concentration of reduced glutathione (GSH) were also estimated. In animals receiving both B(a)P and melatonin, lower levels of MDA+4HDA were observed in all organs as compared to the group treated with B(a)P only. Following administration of B(a)P, GSH level decreased in brain and kidney. Melatonin in combination with B(a)P induced rises in the GSH level in liver and brain, as compared to the receiving B(a)P alone. The activity of SOD increased in the rats treated with melatonin alone but the highest activity was observed in rats treated with B(a)P plus melatonin. CAT activity in the melatonin-treated group increased in brain and liver. Similar to SOD, activity of the enzyme significantly increased in the group treated in combination with B(a)P and melatonin, as compared to the remaining groups in all tested tissues. The results suggest that melatonin protects cells from the damaging action of B(a)P. According to our knowledge, there are no studies describing the effects of melatonin on lipid peroxidation markers and antioxidative enzymes during intoxication of B(a)P in the brain, liver and kidneys. The results of present study give a perspective for further studies of its free radical scavenger properties in prevention of oxidative stress dependent diseases, among others cancers caused by carcinogens such as B(a)P.

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Effects of melatonin on lipid peroxidation and antioxidative enzyme activities in the liver, kidneys and brain of rats administered with benzo(a)pyrene

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