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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 \u03bcg\/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 (<jats:italic>P<\/jats:italic> &lt; 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 \u03bcg\/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\u20131.0 \u03bcg\/g wet wt). Accumulated lead increased significantly (<jats:italic>P<\/jats:italic> &lt; 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 <jats:italic>C. gariepinus<\/jats:italic> are a very sensitive bioassay for aquatic lead pollution. \u00a9 2007 Wiley Periodicals, Inc. 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