No abstract

The effect of lead exposure (100, 300, and 500 microg/L lead nitrate) on embryos of the African catfish Clarias gariepinus were examined by gross morphology and histopathology. Exposition to lead nitrate caused a progressively longer delay in hatching and also reduced the percentage of embryos, which successfully completely hatch from 75% in the control group to 40% in the group exposed to 500 microg/L lead. Categories of gross morphological abnormalities comprised four major ones (irregular head shape, pericardial edema, yolk sac edema, and notochordal defect) and two minor deformations (finfold defect and reduction of pigmentation). The frequencies of recorded morphological malformations increased significantly (P < 0.05) with increasing lead concentration in all stages. Four histopathological categories comprising notochordal defect, gill malformation, eye malformation, and detached skin were recorded. All these malformations were recorded only in the embryos exposed to 300 and 500 microg/L lead. The degrees of histological lesions increased with increasing lead concentration and with length of exposure time. Mean concentrations of lead in the whole embryos were measured and the lowest concentrations of lead were recorded in the control groups (0.3-1.0 microg/g wet wt). Accumulated lead increased significantly (P < 0.05) with increasing dose in all stages. Accumulation of lead in the chorion suggests that the chorion acts as an effective barrier protecting the embryo. Low impact of lead on prehatching stages may be related to both the protective capacity of the chorion and the ability of the perivitelline fluid to concentrate lead. The present results show that (i) lead toxicity was dosage dependent and become evident in gross morphological malformations, followed by histopathological changes, and (ii) early life stages of the African catfish C. gariepinus are a very sensitive bioassay for aquatic lead pollution.

The present study investigates the potential protective effects of tomato paste (9 mg/kg-lycopene) in comparison with vitamin E (50 mg/kg) against the impacts of cadmium (Cd) toxicity (4.64 mg/l: ¼ of 96 h LC50) on fishes Cd exposed for 15 and 30 days. Cd impacts were evaluated in terms of biological, haematological and biochemical characteristics. Cd significantly induced free radicals in serum and liver. The activities of aspartate aminotransferase and alanine aminotransferase in serum were significantly increased due to Cd. Treatment with Cd caused a significant increase in Lipid peroxidation and DNA fragmentation in liver tissue and serum glucose and total lipid. On the other hand, Cd significantly led to decline in serum total protein, blood haemoglobin, red blood cell count, haematocrit value, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration. Dietary supplementation with vitamin E and/or tomato paste to Cd-exposed fish declined significantly the increased lipid peroxidation and DNA fragmentation in liver tissue and the increased aspartate aminotransferase, alanine aminotransferase, glucose and total lipid in serum to the normal condition. This supplementation also significantly increased the declined serum total protein, blood haemoglobin, red blood cell count, haematocrit value, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration to the normal state. Cd impacts and tomato paste/or vitamin E supplementations did not reflected on the condition factor of the fish. These findings demonstrated the beneficial diet supplementation of tomato paste phytonutrients and vitamin E in counteracting the harmful effects of Cd on the characters investigated.