ABSTRACT
Mercury (Hg) is widely distributed in the environment and is known to produce several adverse effects in organisms. The aim of the present study was to examine the in vitro antioxidant activity and Hg chelating ability of the hydroalcoholic extract of Psidium guajava leaves (HEPG). In addition, the potential protective effects of HEPG against Hg(II) were evaluated using a yeast model (Saccharomyces cerevisiae). HEPG was found to exert significant antioxidant activity in 2,2-diphenyl-1-picrylhydrazyl scavenger and inhibition of lipid peroxidation induced by Fe(II) assays in a concentration-dependent manner. The extract also exhibited significant Hg(II) chelating activity. In yeast, Hg(II) induced a significant decrease in cell viability. In contrast, HEPG partially prevented the fall in cell viability induced by Hg(II). In conclusion, HEPG exhibited protective effects against Hg(II)-mediated toxicity, which may be related to both antioxidant and Hg(II)-chelating activities.
Subject(s)
Antioxidants/metabolism , Chelating Agents/metabolism , Mercury/metabolism , Plant Leaves/chemistry , Psidium/chemistry , Saccharomyces cerevisiae/drug effects , Biphenyl Compounds/chemistry , Lipid Peroxidation/drug effects , Picrates/chemistry , Plant Extracts/chemistry , Saccharomyces cerevisiae/physiologyABSTRACT
Methylmercury (MeHg) is a ubiquitous and persistent environmental pollutant that induces serious neurotoxic effects. Diphenyl diselenide [(PhSe)2], an organoseleno compound, exerts protective effects against MeHg toxicity, although the complete mechanism remains unclear. The aim of this study was to investigate the mechanisms involved in the protective effect of (PhSe)2 on the toxicity induced by MeHg using wild-type Saccharomyces cerevisiae and mutants with defects in enzymes and proteins of the antioxidant defense system (yap1Δ, ybp1Δ, ctt1Δ, cat1Δ, sod1Δ, sod2Δ, gsh1Δ, gsh2Δ, gtt1Δ, gtt2Δ, gtt3Δ, gpx1Δ, gpx2Δ, trx1Δ, trx2Δ, trx3Δ, and trr2Δ). In the wild-type strain, (PhSe)2 protected against the growth inhibition, reactive oxygen species production, and decrease in membrane integrity induced by MeHg and restored thiol levels to values indistinguishable from the control. Single deletions of yap1, sod1, sod2, gsh1, gsh2, gpx1, gpx2, trx1, trx2, and trx3 decreased the capacity of (PhSe)2 to prevent MeHg toxicity in yeast, indicating their involvement in (PhSe)2 protection. Together, these results suggest a role of (PhSe)2 in modulating the gene expression of antioxidant enzymes and ABC transporters through the action of the transcription factor YAP1, preventing the oxidative damage caused by MeHg in S. cerevisiae.