Abstract: Melatonin (N-acetyl-5-methoxytryptamine), the main secretory product of the pineal gland, is a free radical scavenger that has been found to protect against lipid peroxidation in many experimental models. In the present study the effect of melatonin on lipid peroxidation of long chain polyunsaturated fatty acids located in rat liver, kidney and brain microsomes was determined using gas chromatography and a chemiluminescence assay. In vitro assays showed that after incubation of rat liver, kidney or brain microsomes in an ascorbate-Fe++ system, at 37 degrees C for 180 min, the total cpm originated from light emission (chemiluminescence) was found to be lower in those membranes incubated in the presence of melatonin. The incubation of rat liver, kidney or brain microsomes in the presence of ascorbate-Fe2+ resulted in lipid-peroxidation of membranes as evidenced by light emission and decrease of docosahexaenoic acid 22:6 n-3 and arachidonic acid 20:4 n-6. In the presence of melatonin (0.5, 1.0, 1.5 mM), light emission percent inhibition of microsomes was: (liver - 3.33, 9.98, 39.40) (kidney - 46.79, 61.88, 68.36) and (brain - 33.36, 28.89, 43.32). Not all fatty acids were equally protected after the addition of melatonin to the incubation medium. Our results indicate a selective protection of C20:4 n6 and C22:6 n3 by melatonin during non-enzymatic lipid peroxidation of rat liver, kidney and brain microsomes. Author Keywords: brain; kidney; lipid peroxidation; liver; melatonin; microsomes
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