NIOSHTIC-2 Publications Search
Antioxidant properties of the pineal neurohormone melatonin in cell-free and lung cell model systems.
Zang-LY; Cosma-G; Gardner-H; Gunselman-S; Vallyathan-V
Toxicologist 1998 Mar; 42(1-S):347
The pineal hormone melatonin exhibits pluripotent biological activities, including modulation of the endocrine, neuroendocrine, and immune systems. Recent evidence has also attributed an antioxidant property to this neurochemical. We have investigated direct quenching of reactive oxygen species by melatonin in cell-free and cell models via electron spin resonance (ESR) studies. Cell-free studies yielded the following information: 1) melatonin inhibited superoxide anion formation with a rate constant of 1.25 x l0(3), M-1s-l in reaction with xanthine/xanthine oxidase; 2) melatonin did not inhibit hydroxyl radical generation in a Fenton reaction; 3) melatonin quenched singlet oxygen produced in a rose bengal photodynamic reaction. On the other hand, melatonin treatments of stimulated alveolar macrophages at physiologic nanomolar concentrations resulted in a dramatic inribition of hydroxyl radical formation (IC-SO = 0.38 nM), moderate inhibition of hydrogen peroxide formation. and no effects on production of superoxide anion. Interestingly, melatonin also inhibited oxidative DNA strand damage/formation of 8-deoxyguanine adducts, as detected by gas chromatography-mass spectrometry, and lipid peroxidation as detected by ELISA, biological effects attributed to inhibition of hydroxyl radical and singlet oxygen, respectively. Ongoing studies are further investigating modulation of DNA transcription factor activities by melatonin.
Hormones; Hormone-activity; Endocrine-system; Endocrine-function; Immune-system; Immune-reaction; Antioxidants; Cell-function; Cellular-reactions; Cellular-structures; DNA-damage
The Toxicologist. Society of Toxicology 37th Annual Meeting, March 1-5,1998, Seattle, Washington
Page last reviewed: April 12, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division