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Effect of Chronic Lead Ingestion by Rats on Glucose Metabolism and Acetylcholine Synthesis in Cerebral Cortex Slices
Author(s) -
Sterling Gerald H.,
O'Neill Kevin J.,
McCafferty Mary R.,
O'Neill John J.
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb03989.x
Subject(s) - metabolism , endocrinology , medicine , bicarbonate , chemistry , carbohydrate metabolism , acetylcholine , ingestion , cerebral cortex , cholinergic , biochemistry , biology
The effect of chronic low‐level lead (Pb 2+ ) ingestion on the metabolic pathways leading to the acetyl moiety of acetylcholine (ACh) was examined. Cerebral cortex slices, prepared from untreated or Pb 2+ ‐exposed rats (600 ppm lead acetate in the drinking water for 20 days), were incubated in Krebs‐Ringer bicarbonate buffer with 10 m M glucose and tracer amounts of [6‐ 3 H]glucose and either [6‐ 14 C]glucose or [3‐ 14 C] β ‐hydroxybutyrate. Altering the concentration of Pb 2+ in the drinking water produced a dose‐related increase in blood and brain lead levels. When tissue from Pb 2+ ‐exposed rats was incubated with mixed‐labeled glucose, incorporation into lacate, citrate, and ACh was considerably decreased, although no changes occurred in the 3 H/ 14 C ratios. Similar effects of Pb 2+ were found when 14 C‐labeled β ‐hydroxy‐butyrate was substituted for the [ 14 C]glucose. It appears from these data that Pb 2+ exerts a generalized effect on energy metabolism and not on a specific step in glucose metabolism. The impairment of glucose metabolism may explain partially the Pb 2+ ‐induced changes observed in cholinergic function.