The Prostatitis Foundation

Melatonin has antioxidant effects


Melatonin has antioxidant effects and may reduce oxidative stress. You may wish to review Dr Shoskes's research on the relationship between oxidative stress and CPPS.

J Pineal Res 1999 May;26(4):236-46
Pharmacological aspects of N-acetyl-5-methoxytryptamine (melatonin) and 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (pinoline) as antioxidants: reduction of oxidative damage in brain region homogenates.
Pless G, Frederiksen TJ, Garcia JJ, Reiter RJ
Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, 78284-7762, USA.
Oxygen consumption is a necessity for all aerobic organisms, but oxygen is also a toxic molecule that leads to the generation of free radicals. The brain consumes a high percentage of the oxygen inhaled (18.5%), and it contains large amounts of unsaturated fatty acids, which makes it highly susceptible to lipid peroxidation. Melatonin (N-acetyl-5-methoxytryptamine), the main secretory product of the pineal gland, is a free radical scavenger that was found to protect against lipid peroxidation in many experimental models. Another compound found in the pineal gland is pinoline (6-methoxy-1,2,3,4-tetrahydro-beta-carboline). Pinoline is structurally related to melatonin. Evidence suggests that pinoline may have an antioxidant capacity similar to that of melatonin.
In this study, the ability of pinoline to protect against H2O2-induced lipid peroxidation of different rat brain homogenates (frontal cortex, striatum, cerebellum, hippocampus, and hypothalamus) was investigated. The degree of lipid peroxidation was assessed by estimating the levels of thiobarbituric acid reactive substances, malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA). Pinoline's antioxidant capacity was compared with that of melatonin. Both melatonin and pinoline reduced the level of MDA and 4-HDA in a dose-dependent manner in all brain regions tested. To compare the antioxidant capacities, percent-inhibition curves were created, and the IC50 values were calculated. The IC50 values for melatonin were higher in all brain regions than were those for pinoline. The IC50 values for melatonin in the five different brain regions ranged from 0.16 mM-0.66 mM, and for pinoline, they ranged from 0.04 mM-0.13 mM.
The possibility of synergistic interactions between melatonin and pinoline were also determined using the method of Berenbaum. Little evidence for either synergistic, additive, or antagonistic interactions between melatonin and pinoline was found.
PMID: 10340726, UI: 99270551

J Urol 1998 Mar;159(3):1069-73
Evidence for a local action of melatonin on the rat prostate.
Gilad E, Laudon M, Matzkin H, Zisapel N
Department of Neurobiochemistry, George S. Wise Faculty of Life Sciences, Tel-Aviv University, Neurim Pharmaceuticals, Israel.
Melatonin, secreted by the pineal gland at night, inhibits pubertal development in rats and possibly humans. We have recently found functional specific binding sites for 125I-labeled melatonin (125I-melatonin) in human benign prostate tissue, localized in the microsomal fraction of the glandular epithelium. The aim of the present study was to set up an animal (rodent) model for the growth inhibitory effects of melatonin on the prostate.
Putative melatonin in the rat ventral prostate were explored by means of autoradiography and receptor binding assays and the ability of melatonin to inhibit stimulated prostate growth was tested in vivo.
In vitro autoradiography and equilibrium binding experiments demonstrated specific binding sites for 125I-labeled melatonin (125I-melatonin) associated with the microsomal fraction of the rat ventral prostate cells (apparent dissociation constant 0.9 nM). 125I-melatonin binding was inhibited by 2-iodomelatonin > 6-hydroxy-melatonin > melatonin = N-(2,4 dinitrophenyl)-5-methoxytryptamine whereas similar concentrations of serotonin, 5-methoxytryptamine, and tryptamine were less potent. The guanine nucleotide analogs, guanosine 5'-0-[3-thiotriphosphate] and guanosine 5'-0-[2-thio-diphosphate], inhibited specific 125I-melatonin binding whereas 5'-guanylyl imido-diphosphate was less potent. Daily injections of testosterone to castrated rats induced regrowth of the prostate and increased the weight of the seminal vesicles. Administration of melatonin to the rats through drinking water prevented the testosterone-mediated regrowth of the prostate but had no effect on the seminal vesicles' weight.
The results demonstrate putative melatonin receptors in the rat prostate and suggest a direct suppression by melatonin of testosterone-dependent prostate growth.
PMID: 9474233, UI: 98134508

Immunology 1999 Feb;96(2):291-297
Prevention of immune dysfunction and vitamin E loss by dehydroepiandrosterone and melatonin supplementation during murine retrovirus infection.
Zhang Z, Araghi-Niknam M, Liang B, Inserra P, Ardestani SK, Jiang S, Chow S, Watson RR
Arizona Prevention Center.
[Record supplied by publisher]
Female C57BL/6 mice infected with the LP-BM5 leukaemia retrovirus developed murine acquired immune-deficiency syndrome (AIDS). Dehydroepiandrosterone (DHEA) and melatonin (MLT) modify immune dysfunction and prevent lipid peroxidation.
We investigated whether DHEA and MLT could prevent immune dysfunction, excessive lipid peroxidation, and tissue vitamin E loss induced by retrovirus infection. Retrovirus infection inhibited the release of T helper 1 (Th1) cytokines, stimulated secretion of Th2 cytokines, increased hepatic lipid peroxidation, and induced vitamin E deficiency. Treatment with DHEA or MLT alone, as well as together, largely prevented the reduction of B- and T-cell proliferation as well as of Th1 cytokine secretion caused by retrovirus infection. Supplementation also suppressed the elevated production of Th2 cytokines stimulated by retrovirus infection. DHEA and MLT simultaneously reduced hepatic lipid peroxidation and prevented vitamin E loss. The use of DHEA plus MLT was more effective in preventing retrovirus-induced immune dysfunction than either DHEA or MLT alone.
These results suggest that supplementation with DHEA and MLT may prevent cytokine dysregulation, lipid oxidation and tissue vitamin E loss induced by retrovirus infection. Similarly, hormone supplementation also modified immune function and increased tissue vitamin E levels in uninfected mice.
PMID: 10233708


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