Prophylactic action of melatonin against cyclophosphamide-induced oxidative stress in mice

Abstract

The present study investigated the prophylactic influence of melatonin against cyclophosphamide-induced oxidative stress in mouse tissues. Lipid peroxidation, reduced glutathione (GSH), glutathione disulphide (GSSG), glutathione peroxidase (GSH-Px) and serum phosphatase levels were analyzed in brain, spleen liver, lungs, kidney and testes. Fifteen days oral administration with melatonin (0.1 mg/kg bw per day) before treatment checked the augmentation of the level of lipid peroxidation, blood GSSG and acid phosphatase caused by an acute treatment with a radiomimetic drug, cyclophosphamide (75 mg/kg bw). Cyclophosphamide-induced depletion in the level of GSH, GSH-Px and alkaline phosphatase was made up statistically significant by chronic melatonin administration given orally. The results indicate the antioxidative properties of melatonin resulting into its prophylactic property against the cyclophosphamide-induced biochemical alterations. The finding support the idea that melatonin is a potent free-radical scavenger and antioxidant.

Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy

“…CP is a prodrug, which must be metabolically activated, mainly in the liver, into its DNA alkylating cytotoxic form. CP treatments have also been shown to increase the generation of reactive oxygen species (ROS) and oxidative DNA damage (8-hydroxyguanosine) in human granulosa cells (20) and to induce oxidative stress and lipid peroxidation as well as GSH reduction (21). As a very simple model system to understand the differential effect of STS on the mixture of normal and cancer cells observed in mammals with metastatic cancer, we mixed in the same flask mutants lacking SCH9 with mutants lacking SCH9 but also expressing RAS2 val19 at a 25:1 ratio and exposed them to chronic treatment with CP or MMS.…”

Protective Effect of Seleno-l-Methionine on Cyclophosphamide-Induced Urinary Bladder Toxicity in Rats

“…All sections were examined under ×40 objective and scored for edema, hemorrhage, and inflammation on a scale of 0 (normal) to 3 (severe changes). Mucosal ulceration was scored as 0 (normal), 1 (epithelial denuding), 2 (focal ulceration), and 3 (widespread epithelial ulceration) [5][6][7][9][10][11][12][13][14][15][16].…”

“…Numerous studies have shown that CP exposure enhances intracellular ROS production, suggesting that biochemical and physiological disturbances may result from oxidative stress [9]. The antioxidative defense system includes enzymes, such as glutathione peroxidase (GPx), superoxide dismutase, catalase [10], and non-enzyme antioxidants, like carotenoids [11] and selenium [12].…”

Protective Effect of Carvacrol Against Oxidative Stress and Heart Injury in Cyclophosphamide-Induced Cardiotoxicity in Rat

“…By modulating the DNA synthesis, CP prevents cellular proliferation (Dollery 1999). Numerous studies have shown that CP exposureenhances intracellular reactive oxygen species (ROS) production, suggesting that biochemical and physiological side effects may result from its oxidative stress (Manda and Bhatia 2003). Shanholtz (2001) found out that there was a fatal cardioxicity when CP was administrated at high doses.…”