Abstract

With a view to investigate whether in-ovo cadmium (Cd) exposure can attribute toxic effects in developing avian embryo, the fertile eggs of Japanese quail were injected with Cd and the mortality during incubation and the body weights of day-old hatchlings were measured. The Cd toxicity in the embryo were also assessed by evaluating some well-known oxidative stress markers such as metallothionein (MT) mRNA expression, catalase activity and malondialdehyde (MDA) production in day-10 male and female embryos exposed to Cd with or without ascorbic acid. Results showed that as minimum as 1μg/egg of in-ovo Cd administration increased the embryonic death and decreased the hatchling body weights. A slightly higher mortality rate was found in the 1μg Cd/egg received male embryos than in the female embryos. Compare to the control, higher MT mRNA expression and MDA generation were observed in 1μg Cd/egg received live embryos irrespective of sex. Co-exposure of 50μg ascorbic acid with 1μg Cd/egg inhibited the increse in MDA production in embryos of both sexes but the augment of MT mRNA expression was supressed only in female embryos. These results suggested that in-ovo Cd pollution in avian species might cause the embryonic toxicity leading to death, and the sensitivity of developing quail embryo to antioxidant protection against Cd toxicity is not exactly similar in both sexes of embryos.

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