Modulation of antioxidant defences in digestive gland of Perna viridis (L.), on mercury exposures.
Sub-lethal effects of mercury exposure (110th of LC(50), i.e. 0.045 mg l(-1)) for 5, 10 and 15 d was investigated on oxidative stress parameters and antioxidant defences in digestive gland of Perna viridis. In addition to this an in vitro effect of mercury single and supplemented with reduced glutathione on lipid peroxidation was studied. Increased lipid peroxidation (during first 10 days and also during in vitro exposures), protein carbonyl and hydrogen peroxides (from 5th till last day of exposure) indicate the resultant oxidative stress in the mercury exposed specimen. DNA damage (F-value) response although less distinct on 5th and 15th d, its low values on 10th d and significant correlation with hydrogen peroxide suggests the toxic role of free radicals towards DNA integrity. Superoxide dismutase, which remains low initially (5th d) and increases later suggests its immediate response against superoxide radical. Higher activities of catalase, glutathione peroxidase and glutathione reductase on 15th d and glutathione-S-tranferase from 10th d onwards suggests the adaptive behaviour of the tissue against oxyradicals. Increasing levels of non-enzymatic antioxidant molecules, such as reduced glutathione and ascorbic acid indicated its involvement in counteracting oxidative damage. Further role of reduced glutathione in reducing Hg toxicity is evident in in vitro experiments where lipid peroxidation remains low in mercury concentrations supplemented with reduced glutathione. The elevated levels of metallothionein from 5th to 10th d suggest involvement of this protein in detoxification of reactive oxygen species and toxic metal. The above results suggest that both enzymatic and non-enzymatic antioxidants play an important role in protecting cell against Hg toxicity, which can be used as a biomarker of metal contamination in aquatic environment.
Verlecar
X N
XN
Environmental Laboratory, Biological Oceanography Division, National Institute of Oceanography, Dona Paula, Goa 403004, India. verlecar@nio.org
Jena
K B
KB
Chainy
G B N
GB
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004064:Digestive System / Q000187:drug effects* / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase; D006861:Hydrogen Peroxide / Q000378:metabolism; D008628:Mercury / Q000633:toxicity*; D008668:Metallothionein / Q000378:metabolism; D049883:Perna / Q000187:drug effects* / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D014874:Water Pollutants, Chemical; D008668:Metallothionein; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D008628:Mercury; D005978:Glutathione; D001205:Ascorbic Acid