Autoxidation and toxicant-induced oxidation of lipid and DNA in monkey liver: Reduction of molecular damage by melatonin

Javier Cabrera, Susanne Burkhardt, Dun Xian Tan, Lucien C. Manchester, Malgorzata Karbownik, Russel J. Reiter

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Melatonin, the main secretory product of the pineal gland, is a free radical scavenger and antioxidant which protects against oxidative damage due to a variety of toxicants. However, there is little information regarding melatonin's antioxidative capacity in tissues of primates. In this study we examined the protective effects of melatonin in monkey liver homogenates against lipid damage that occurred as a result of autoxidation or that induced by exogenous addition of H2O2 and ferrous iron (Fe2+). Additionally, we tested melatonin's protective effect against oxidative damage to DNA induced by chromium(III) (CrIII) plus H2O2. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of lipid peroxidation, and the concentrations of 8-hydroxydeoxyguanosine (8-OHdG) as an endpoint of oxidative DNA damage. The increases in malondialdehyde +4-hydroxyalkenals concentrations as a consequence of autoxidation or after the addition of H2O2 plus Fe2+ to the homogenates were time-dependent. The accumulation of these damaged products due to either autoxidative processes or induced by H2O2 and Fe2+ were significantly reduced by melatonin in a concentration-dependent-manner. The levels of 8-OHdG were elevated in purified monkey liver DNA incubated with a combination of CrCl3 plus H2O2. This rise in oxidatively damaged DNA was prevented by 10 μM concentration of melatonin. Also, melatonin reduced the damage to DNA that was caused by autoxidative processes. These findings in monkey liver tissue document the ability of melatonin to protect against oxidative damage to both lipid and DNA in primate tissue, as observed previously in rodent tissue. The findings provide support for the use of melatonin as suitable agent to reduce damage inflicted by free radical species in primates.

Original languageEnglish (US)
Pages (from-to)225-230
Number of pages6
JournalPharmacology and Toxicology
Volume89
Issue number5
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Health, Toxicology and Mutagenesis

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