Samuel Patrick Ozovehe1*, Arimoro FO1, Ayanwale AV1, Mohammad HL2
The anthropogenic activities culminating in environmental pollution all over the world that usually leads to release of plethora of pollutants such as cadmium calls for concern. In the present study the effects of cadmium chloride on the production of antioxidants such as Malondialdehyde (MDA) in C. gariepinus and how such effects can be ameliorated through administration of vitamins were investigated. C. gariepinus fingerlings (whose initial weight ranged from 3-11 g) were exposed to sub-lethal concentrations of Cd (00, 12 mg/L, 16 mg/L, 20 mg/L and 24 mg/L) with replicate in each case. Minimum concentration of the toxicant was taken as the concentration for each of the vitamins and administered across all bud. Fresh concentrations of both toxicant and vitamins were administered every 72 hours for a period of 12 weeks every time the water medium was changed. The various treatments group include Cd (Cd only with T1-T4 and replicates), CdVA (Cd+vitamin A with T1-T4 and replicates), CdVC (Cd+vitamin C with T1-T4 and replicates) and CdVE (Cd+vitamin E with T1-T4 and replicates). 3 samples of the fish were randomly selected and sacrificed from each aquarium tank every 2 weeks of the exposure period. The gills, kidneys and liver were excised from these specimens and homogenized in sodium phosphate buffer. From the results: samples exposed to Cd only group, the MDA production levels in the liver were generally low. The T2 and T3 mean values in the 6th and 10th weeks of exposure, respectively are significantly higher than other treatments including the control. The control mean values in the 8th week of exposure are significantly higher than other treatments. The highest mean value of MDA in the liver was 40.17 ± 0.05 nM/mg obtained in T3 at the end of the 2nd week of exposure. In the kidney, the control mean values in the 2nd, 4th, 8th and 10th weeks of exposure, respectively are significantly higher than other treatments. The T4 mean values in the 6th week of exposure are significantly higher than other treatments. The highest MDA mean value in this regard, was 40.05 ± 0.03 nM/mg obtained in T4 at the end of the 6th week of exposure. The control mean values in the gill of the samples are significantly higher than other treatments in the 2nd week of exposure. The T3 and T1 mean values in the 4th and 6th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the gill was 34.98 ± 0.02 nM/mg obtained in T1 at the end of the 6th week of exposure. In the samples exposed to CdVA, MDA production levels in the liver were generally low. The T3 mean values in the 6th and 8th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the liver was 39.52 ± 0.05 nM/mg obtained in T3 at the end of the 6th week of exposure. The T2 and T3 mean values in the 2nd and 4th weeks of exposure, respectively are significantly higher than other treatments. The T3 mean values in the 8th week of exposure are significantly higher than other treatments. The highest MDA mean value in the kidney in this regard, was 41.23 ± 0.34 nM/mg obtained in T3 at the end of the 4th week of exposure. The T1 and T3 mean values in the gill of the samples are significantly higher than other treatments in the 2nd and 4th weeks of exposure, respectively. The highest mean value of MDA in the gill was 40.07 ± 0.05 nM/mg obtained in T3 at the end of the 4th week of exposure. From the samples exposed to CdVC, MDA production levels in the liver indicated that T1 and T2 mean values, respectively are significantly higher than other treatments in the 2nd and 4th weeks of exposure. The T1 and T2 in the 10th and 12th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the liver was 40.03 ± 0.05 nM/mg obtained in T4 at the end of the 6th week of exposure. The kidney’s T1, T2 and T3 mean values in the 2nd, 4th and 6th weeks of exposure, respectively are significantly higher than other treatments. The T2 mean values in the 8th, 10th and 12th weeks of exposure, respectively are significantly higher than other treatments. The highest MDA mean value in this regard, was 36.67 ± 0.03 nM/mg obtained in T2 at the end of the 4th week of exposure. T1 and T2 mean values in the 10th and 12th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the gill was 39.54 ± 0.06 nM/mg obtained in T1 at the end of the 10th week of exposure. From the results of the samples exposed CdVE, MDA production levels in the liver indicated that T1 mean values are significantly higher than other treatments in both 2nd and 4th weeks of exposure, respectively. The T2 and T3 mean values in the 6th and 8th weeks of exposure, respectively are significantly higher than other treatments. T2 mean values in the 10th and 12th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the liver was 58.62 ± 0.03 nM/mg obtained in T2 at the end of the 6th week of exposure. The T1 and T3 mean values in the 2nd and 4th weeks of exposure, respectively are significantly higher than other treatments. The T4 and T2 mean values in the 8th and 10th weeks of exposure, respectively are significantly higher than other treatments. The highest MDA mean value in this regard, was 39.17 ± 0.03 nM/mg obtained in T3 at the end of the 4th week of exposure. The T2 and T1 mean values in the gill of the samples are significantly higher than other treatments in the 2nd and 4th weeks of exposure, respectively. T2 mean values in both 10th and 12th weeks of exposure, respectively are significantly higher than other treatments. The highest mean value of MDA in the gill was 36.81 ± 0.03 nM/mg obtained in T2 at the end of the 2nd week of exposure. The fish samples exposed to the toxicant displayed slight variations in the treatment groups and in all the organs of interest except in the CdVE group where the highest production of the antioxidant was obtained in the liver in response to the effects of the toxicant. Higher concentrations of the vitamins could facilitate better understanding of the ameliorative roles of the vitamins.
