Triethyllead‐induced peroxidative damage in various regions of the rat brain

Abstract

Adult male Fisher 344 rats (8-10 wk old) were dosed ip with 1.75 mg/kg body weight of triethyllead chloride (TEL) for 5 consecutive days. Rats were sacrificed 1, 7, or 21 d after the last injection. The rate of lipid peroxidation was significantly elevated in frontal cortex at all three time points assayed (1, 7, or 21 d). However, hippocampal and cerebellar membranes showed no changes in peroxidative capacity at these time points. In order to determine whether cortical membrane damage was reflected in alteration of a restricted protein population, a series of high-affinity receptor binding sites was determined in cortical membranes derived from treated rats 7 d after the last injection of triethyllead. The rate of lipid peroxidation was significantly increased in the frontal cortex of triethyllead treated rats; however, no changes in the binding of [3H]spiroperidol, [3H]quinuclidinyl benzilate, and [3H]benzodiazepine were seen in animals exposed to triethyllead. The cortical wet weight, protein content, and cell number were also unchanged by TEL treatment, reflecting an absence of gross damage.

Lead Accumulation in the Bones of Aging Male Mice

“…Most studies indicate a relationship between low level lead exposure and hypertension in humans and animals [Fine et al, 1988;Harlan, 1988;Kromhout, 1988;Perry et al, 1988;Victery, 1988] while one study does not [Selevan et al, 1988], Low level lead exposure affects the electrical and mechanical activity of the heart in animals [Kopp et al 1988], Atherosclerosis can be induced by lead ions [Revis et al, 1981]. Lead ions can induce lipid peroxidation [Quinlan et al, 1988;Ali and Bondy, 1989], Lead expo sure results in decreased antibody formation in mice [Roller and Kovacic, 1974], High concentrations of lead have been found in senile cataractous human lenses [Racz and Erdohelyi, 1988], Behavior impairment in both monkeys [Gilbert and Rice, 1987] and humans [Needleman et al, 1990] appears to be a persistent legacy of low level lead expo sure. It, therefore, seems reasonable to as sume that low level lead exposure would have negative effects in general.…”

Ethanol toxicity and oxidative stress

“…Evidence for this comes from human exposures which have been associated with elevated levels of superoxide dismutase, presumably induced by oxidative stress [2], and by animal studies [3,4]. Organic lead compounds have also been reported to elevate levels of lipid peroxidation in tissues of treated animals [5][6][7]. However, demonstration of the pro-oxidant capacities of lead using isolated preparations has not been unequivocally made; lipid peroxidation can in fact be inhibited under such circumstances [7].…”