Hydrogen Sulphide Exposure on Lipid Peroxidation and Antioxidant Enzymes in Fishes
Abstract: Oxidative stress may ensue when the ability to buffer against reactive oxygen species (ROS) is exceeded either by excessive production of ROS or by depletion of antioxidant. This can alter cellular redox-poise and initiate a variety of responses via intracellular pathways. Hydrogen sulphide is a toxic gas which is harmful to aquatic organisms especially in the unionized form. In the present study two different concentrations of hydrogen sulphide is used for the toxicity assay in two test groups of Oreochromis mossambicus in time intervals of 12hrs, 24 hrs, 48hrs, 72 hrs and 96 hrs. With respect to the H2S concentration and duration of exposure, alterations were recorded in the concentration of lipid peroxidation products and antioxidants in the various organs of the test fishes. Malondialdehyde content increases in liver, gill, kidney and brain on exposure to hydrogen sulphide up to 48hrs and then the MDA content showed steady value up to 98hrs experimental period. Brain and kidney showed the maximum increase in concentration of reduced glutathione in initial stages (48 hrs) of hydrogen sulphide treatment. The gradual decrease in concentration of GSH in the tissues of H2S exposed fishes after 48 hrs up to 96hrs compared to the control shows the loss of adaptive mechanisms and the oxidation of GSH to GSSG. Slight increase in the activity of glutathione-S-transferase and decrease in activity of glutathione peroxidase demonstrated the incapability of the vital organs in neutralizing the peroxides generated in the oxidative stress condition.
Keywords: Oxidative stress, lipid peroxidation, hydrogen sulphide, antioxidants, malondialdehyde
How to Cite?: Sreejai R., Chithra V. S., "Hydrogen Sulphide Exposure on Lipid Peroxidation and Antioxidant Enzymes in Fishes", Volume 5 Issue 6, June 2016, International Journal of Science and Research (IJSR), Pages: 356-361, https://www.ijsr.net/getabstract.php?paperid=NOV164040, DOI: https://dx.doi.org/10.21275/NOV164040