The influence of melatonin and N-acetylcysteine in delta-aminolevulinic acid and lead induced genotoxicity in lymphocytes in vitro

Uestundag A., Duydu Y.

BIOLOGICAL TRACE ELEMENT RESEARCH, vol.117, no.1-3, pp.53-64, 2007 (SCI-Expanded, Scopus) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 117 Issue: 1-3
  • Publication Date: 2007
  • Doi Number: 10.1007/bf02698083
  • Journal Name: BIOLOGICAL TRACE ELEMENT RESEARCH
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.53-64
  • Keywords: antioxiclants, genotoxicity of ALA, genotoxicity of lead, micronucleus, sister chromatid exchange, SISTER-CHROMATID EXCHANGE, OXIDATIVE STRESS, HOMOLOGOUS RECOMBINATION, EXPOSURE, INHIBITION, BIOMARKER, PROTECTS, WORKERS, CELLS
  • Ankara University Affiliated: Yes

Abstract

As is well known from earlier studies, the genotoxic effect of lead exposure was partly attributed to the formation of the highly reactive oxygen metabolites (ROMs) in the blood. However, lead ions have no ability to generate ROMs. Therefore, the recently published studies paid more attention to the role of delta-aminolevulinic acid (ALA) accumulation in lead-induced DNA damage. If the above-mentioned assumptions were taken into consideration, it seemed a reasonable approach to study the possible protective effects of antioxidants against genotoxic effects of lead. According to our results, N-acetylcysteine (NAC) and melatonin (MEL) were able to reduce significantly (p < 0.05) the lead- and ALA-induced sister chromatid exchange frequencies in human lymphocytes in vitro. In spite of a relative reduction in the lead- and ALA-induced micronucleus formation in human lymphocytes, the reduction was not statistically significant (p > 0.05). These results could be evaluated as supportive evidence for the hypothesis that increased antioxidant capacity of cells might fortify the efficiency of protective pathways against cytogenetic damage in lead exposure.