title: Ontogenic profile of brain lipids following perinatal exposure to cadmium.
abstract: Uniparous female rats were exposed to 10 ppm cadmium (as Cd(CH3COO)2) in drinking water, ad libitum, from day 0 of pregnancy; neonates exposed to Cd gestationally and lactationally were separated from their mothers at 21 days of age and were given 10 ppm Cd in drinking water up to 45 days of age. The sequential analysis of brain lipids during development showed a significant reduction in the total lipid levels at 15, 21, 30 and 45 days of age compared to the respective controls. No change in the triglyceride levels was observed in the Cd-exposed group, except for a slight but statistically significant increase (12%, p < 0.05) at day 15 of postnatal life. Metallic exposure also decreased the cholesterol content of brain at different time intervals in comparison to its levels in age-matched control rats. The analysis of sialic acid content of the total gangliosides revealed elevated levels of this group of glycolipids at 21 (25%), 30 (17%) and 45 (23%) days of age compared to their counterpart controls. However, a remarkable reduction in the concentration of brain galactosylceramide (30-43%) and 3'-sulphogalactosylceramide (24-37%) at 21, 30 and 45 days of age was observed following pre- and postnatal exposure of cadmium in comparison to the respective controls. The ontogenic profile of different brain phospholipids in the Cd-exposed group showed an increase in the levels of phosphatidylethanolamine at 21 (31%), 30 (25%) and 45 (19%) days of age; the phosphatidylcholine contents increased at day 21 (14%), followed by a significant decrease at 30 (14%) and 45 (19%) days compared to age-matched controls. Brain phosphatidylinositol, phosphatidylserine and sphingomyelin did not show any alteration at early periods of exposure but decreased significantly following continued exposure by 34%, 45% and 21%, respectively, at 45 days of age. Metal analysis in the brain showed a reduction in zinc and copper levels at 15 and 21 days of age in Cd-exposed animals; however, iron levels remained comparable with control values throughout the experiment. It may be concluded that an early exposure of Cd may produce alteration in the development of different lipids, which may produce CNS dysfunctions with a possibility of being manifested even in later life.
authors.affiliation: Neurotoxicology Research Group, Industrial Toxicology Research Centre, Lucknow, India.
authors.forename: A
authors.initials: A
authors.lastname: Gupta
authors.forename: G S
authors.initials: GS
authors.lastname: Shukla
mesh_terms: D000085:Acetates / Q000633:toxicity*; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development*; D000833:Animals, Suckling / Q000254:growth & development; D001921:Brain / Q000187:drug effects* / Q000254:growth & development*; D001923:Brain Chemistry / Q000187:drug effects*; D002104:Cadmium / Q000633:toxicity*; D005260:Female; D007774:Lactation / Q000187:drug effects; D050356:Lipid Metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000085:Acetates; D002104:Cadmium; C028031:cadmium acetate