Abstract

Cadmium is a potent teratogen in laboratory animals, causing exencephaly when administered at early stages of development. Due to its heterogenicity with respect to molecular targets, the mechanisms behind cadmium toxicity are not well understood. In the present study, 40 pregnant rats (Sprague-Dawley) were divided into four groups (10 each); first group served as the control (G1), the second group (G2) received 61.3 mg/kg cadmium chloride daily from 7th to 16th day of gestation (organogenesis period) by oral tube. Group 3 (G3) was administrated a solution of 25 mg/kg zinc chloride orally from the 1st day to 20th day of pregnancy. Group 4 were administrated a solution of cadmium chloride (61.3 mg/kg) and zinc chloride (25 mg /kg) daily from the 7th to16th day of gestation. Maternal body weights were measured on gestational day 0, 6, 9, 12, 15 and 20. At the 20th day of gestation, blood samples were collected from the eye, using orbital sinus technique. Serum aspartate transaminase (AST) and alanine transaminase (ALT) were determined calorimetrically and serum, urea and creatinine were determined. All of the pregnant rats were sacrificed by ether anaesthesia at the 20^th day of gestation and foetuses were removed from the uterus. The implantation sites, corpora lutea, living, dead and reabsorbed foetuses were counted and recorded. Liver of pregnant rats and their fetuses were used to isolate a total RNA for quantification of Msx1, Cx43, Bcl2 and Bax genes. The results show the toxic effect of Cd on the pregnant rats and their fetuses, at morphological, physiological and molecular level but, zinc has a very effective protection against cadmium-induced developmental toxicity.

Key words: Cadmium, zinc, rat, organogenesis, gene expression.