THERAPEUTIC EFFECT OF L-ASCORBIC ACID ON LEAD NITRATE INDUCED PATHOLOGY IN SOME ORGANS OF THE AFRICAN CATFISH Clarias gariepinus

SOURCE:

Faculty: Biosences
Department: Zoology

CONTRIBUTORS:

Ikeogu, C. F.
Nsofor, C. I.

ABSTRACT:

The objective of the study was to determine the toxic effects of sub lethal concentrations of lead nitrate, its tissue residues, and the possible therapeutic effects of L-ascorbic acid on lead nitrate toxicity in Clarias gariepinus. This study was based on 48 hours acute toxicity tests carried out on four Clarias gariepinus juveniles of mean weight 39.80±1.54g and mean length 21.05± 1.23cm. The LC50 of lead nitrate was 60mg/l.The LC50 of vitamin C (Kepro®) was 175mg/l. Sublethal concentrations of 0,5,10, and 15mg/l lead nitrate were employed in experiment 1 investigating the chronic effects of lead nitrate on Clarias gariepinus juveniles for 91 days (13 weeks). 50 and 100mg/l of kepro® vitamin C powder were employed as bath treatment to the 91 day lead exposed experimental fish for 7 days. The effects of lead nitrate on haematological parameters; PCV, RBC count, Hb concentration, TWBC count, and DWBC were assessed using standard methods before lead exposure to obtain day zero data, after 91 day lead exposure, and after 7 day treatment with 50 and 100mg/l kepro® vitamin C. Biochemical parameters investigated were serum enzymes: AST, ALT, ALP and urea. The histology of the gills, liver, and stomach were also carried out to assess the histopathological effects of 91 day exposure to lead nitrate and 7 days treatment with vitamin C on these organs. Haematology, enzymology and histology of the gills, liver and stomach of Clarias gariepinus were also carried out with concurrent exposure to lead nitrate and vitamin C in experiment 2 for 91 days to assess the effects of vitamin C on the chronic effects of lead nitrate on the blood, serum enzymes, gills, liver, and stomach of Clarias gariepinus in the same aquaria. Lead accumulation in the muscles of Clarias gariepinus was determined in both experiments through A.A S. Results of experiment 1 showed significant decrease (P<0.05) in PCV, Hb, and RBC of 91 day lead nitrate exposed groups when compared to day zero and control groups. This signifies anaemia. A significant increase (P<0.05) in TWBC in the fish exposed to varying concentrations of lead when compared to the control and day zero group is termed leucocytosis. Enzymes assay showed significant decrease (P<0.05) in AST, ALT and ALP levels in the lead nitrate exposed groups when compared to the control. A significant increase (P<0.05) in the urea of the lead nitrate exposed group when compared to the control group is termed azotemia and is an indication of poor renal function. There was a significant increase in the concentration of lead in the muscle of the lead exposed groups when compared to the control group. The histology of gills showed distorted lamellae, necrotic primary and secondary lamellae, severely damaged lamellae in the lead exposed groups when compared to the control a group. The liver histology of Clarias gariepinus exposed to varying concentrations of lead nitrate showed cytoplasmic vacuolations,pyknotic nuclei and degenerated hepatocytes. The liver of the control showed normal liver parenchymal cells. The histology of the stomach of Clarias gariepinus exposed to varying concentrations of lead nitrate showed mucosal haemorrhages, broken crypts and degeneration of the columnar epithelial cells of the mucosa, when compared to the normal cells of the control. The results of the 7 day treatment of the lead exposed groups with 50mg/l and 100mg/l vitamin C showed a significant increase (P<0.05) in PCV,Hb and RBC between the exposed and treated groups. There was no significant difference (P>0.05) between the 50mg/l vitamin C and 100mg/l vitamin C groups. Treatment of the lead nitrate exposed group with vitamin C showed that there was no significant difference (P>0.05) between the TWBC of exposed and treated groups and between the 50mg/l vitamin C and 100mg/l vitamin C. Treatment of the lead nitrate exposed group with vitamin C showed a significant decrease (P<0.05) in AST, ALT and ALP between the lead exposed groups and the vitamin C treated groups. Treatment of lead exposed group showed a significant decrease (P<0.05) in urea level between the lead exposed group and vitaminC treated groups. The 100mg/l vitamin C showed more significant decrease (P<0.05) in urea level than the 50mg/l vitamin C. The histopathology of the gills, liver and stomach caused by lead nitrate toxicity was significantly resolved (P<0.05) when treated with 50mg/l vitamin C and 100mg/l vitamin C with 50mg/l vitamin C having better therapeutic effect than 100mg/L vitamin C. There was a significant decrease (P<0.05) in lead accumulated in fish muscle after treatment of the lead nitrate exposed group with vitamin C. The 50mg/l vitamin C was more effective in reducing lead level in the muscle of the exposed fish than the 100mg/l.Results of experiment 2 showed that there was no significant difference (P>0.05) between the pathology of Clarias gariepinus exposed to lead nitrate and the group exposed concurrently to lead and vitamin C. The toxicity of lead nitrate could not be reversed by Vitamin C during concurrent exposure. The study concluded that lead is toxic to Clarias gariepinus at sublethal concentrations and that vitamin C at the water bath dose of 50mg/l administered for 7 days can reverse the damaging effects of lead on fish. It is therefore recommended that fish from lead polluted waters can be made safe by treatment with 50mg/l vitamin C for 7 days. Also bioaccumulated lead residues in the muscles of lead contaminated fish can significantly be reduced by 50mg/l Vitamin C for 7 days as a food safety measure.