Ethanol self-administration in rats following exposure to dietary cadmium

Nation, Jack R.; Baker, Dorothy M.; Bratton, Gerald R.; Fantasia, M. A.; Andrews, Karolyn M.; Womac, Carolyn

doi:10.1016/0892-0362(87)90028-6

Cited by 20 publications

(11 citation statements)

References 26 publications

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“…Cadmium (Cd +2 ) is a potentially toxic element being ubiquitously present in environments to which humans and animals are exposed via a variety of routes, including industrial contamination, food sources, and tobacco smoke (Nation et al 1987;Hudecova and Ginter 1992). Inhibition of bioamine uptake, Na-K ATPase, and voltagedependent Ca +2 channels are among the numerous effects of Cd +2 poisoning.…”

Section: Introductionmentioning

confidence: 99%

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

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Ballı

et al. 2009

Toxicology Mechanisms and Methods

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In this study, the systemic hemodynamics induced by acute and chronic cadmium (Cd+2) intoxication in the cardiovascular system of rats using thoracic electrical bioimpedance were examined and the acute and chronic effects of Cd+2 intoxication on the activities of antioxidant enzymes and malondialdehyde (MDA) were compared. Also, in this study, ultrastructural changes in the heart and aorta of rats were evaluated. Thirty-eight male Wistar albino rats were randomly divided into control, acute, and chronic groups. Chronic group was administered by oral gavage an aqueous solution of CdCl2 for 60 days, at dose of 15 mg Cd+2/kg/day. Acute group was administered by oral gavage an aqueous solution of CdCl2 with a single dose of 15 mg Cd+2/kg. Cadmium increased the stroke volume and cardiac output of rats in the chronic group, but did not change the heart rate significantly. Antioxidant enzymes activities and MDA level significantly increased in the chronic group. In ultrastructural examination, there were widespread degenerative changes in heart muscle cells of the chronic group but endothelial cells and smooth muscle cells in the aorta tissue samples had normal morphological features in all groups. All of the findings indicate that Cd+2 toxication can cause deformation in heart muscle cells due to an increase in free radicals and lipid peroxidation. Also, this study has confirmed that a long-term-Cd+2 exposure increased stroke volume (SV) and cardiac output (CO), but did not change the heart rate (HR).

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Section: Introductionmentioning

confidence: 99%

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Ozturk

Büyükakıllı

Ballı

et al. 2009

Toxicology Mechanisms and Methods

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“…After each rat had been sacrificed, trunk blood was collected. The concentration of cadmium in the blood was obtained through dry ashing and atomic absorption spectrophotometry, as described elsewhere (Nation et al, 1987).…”

Section: Chemical Analysismentioning

confidence: 99%

“…Evidence of cadmium-based disturbances in transmitter processes has stimulated interest in other areas in which such chemical events play a regulatory role. In the laboratory, issues relating to the interaction of cadmium and psychoactive drugs such as ethanol (e.g., Nation et al, 1987Nation et al, , 1988Nation, Frye, Von Stultz, & Bratton, 1989;Nation, Horger, Pugh, Bratton, & Rowe, 1990) and cocaine (Nation et al, 1991) have been a central concern. With regard to the effects of cotreatment with cadmium and ethanol, chronic exposure to inorganic cadmium stimulates increased volitional intake of a nonpreferred ethanol solution (Nation et al, 1987;Nation, Pugh, Von Stultz, Bratton, & Clark, 1989) but attenuates responsiveness to acute applications of the drug.…”

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confidence: 99%

“…In the laboratory, issues relating to the interaction of cadmium and psychoactive drugs such as ethanol (e.g., Nation et al, 1987Nation et al, , 1988Nation, Frye, Von Stultz, & Bratton, 1989;Nation, Horger, Pugh, Bratton, & Rowe, 1990) and cocaine (Nation et al, 1991) have been a central concern. With regard to the effects of cotreatment with cadmium and ethanol, chronic exposure to inorganic cadmium stimulates increased volitional intake of a nonpreferred ethanol solution (Nation et al, 1987;Nation, Pugh, Von Stultz, Bratton, & Clark, 1989) but attenuates responsiveness to acute applications of the drug. For example, cadmium-burdened animals exhibit a hyposensitivity to ethanol in studies in which a hypnotic dose of the drug is administered (Nation et al, 1988), in tests of ethanol's hypoalgesic effects (Burkey, Nation, Grover, & Bratton, 1993), and in ethanol self-administration paradigms in which animals lever press for ethanol reinforcement (Grover et al, 1991).…”

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confidence: 99%

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Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

Nation¹,

Burkey²,

Bratton³

1995

Experimental and Clinical Psychopharmacology

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Twelve rats exposed to water containing 100 ppm cadmium and 12 control rats received intraperitoneal injections of 0.5, 1.0, and 1.5 g/kg ethanol prior to activity testing. Eleven rats exposed to cadmium and 11 control rats received comparable injections of saline prior to activity testing. In addition, all rats were tested on a rota-rod task. Activity results showed that parallel behavioral decreases occurred for cadmium-treated and control subjects. However, cadmium attenuated ethanol-induced impairment of rota-rod performance. These data indicate that the external chemical environment may alter drug responsiveness.Editor's Note. Because of unexpected delays with the editor's office, the publication of this article was postponed beyond its originally scheduled issue. The editor apologizes for the delay.-CRS

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“…In their adult years, thes poorer reading scores, are clumsier, have more evidence of depression, and tend to have a higher rate of hard drug use. With regard to the last observation, is Nation's report that rats, which ordinarily find alcohol aversive, when given lead, will significantly increase their intake of alcohol (26). Under funding from NIEHS, we will study the effects of lead exposure on school outcome, attention deficit disorder, and social adaptation.…”

Section: Academic and Social Costs Of Silent Lead Exposurementioning

confidence: 99%

The future challenge of lead toxicity.

Needleman

1990

Environ Health Perspect

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Five decades ago, lead toxicity in childhood was thought in nonlethal cases to be without residual effect. This misconception was corrected in 1943 by Randolph Byers, who began the modern era of lead neurotoxicology by asserting that lead not only killed cells, but interfered with the normal development of central nervous system neurons. The human data from Byers forward is reviewed, with particular attention on methodological issues that have emerged. The papers on human neurotoxicology presented at the NIEHS lead conference held in Research Triangle Park, NC, in 1974 are examined to demonstrate the progress made over the last 15 years. Seven methodological solecisms have clouded judgment over the question of lead toxicity at low dose: worship of the sacrament of p = 0.05; inaccurate causal modeling; drawing conclusions from studies with inadequate power; positing phantom covariates; underestimating the importance of "small" effects; demanding proof of causality; and evaluating studies in isolation. The principles behind these errors are discussed. Lead exposure is associated with hyperactivity, and hyperactivity is a risk factor for antisocial behavior. The relationship between lead exposure and antisocial behavior is estimated. A plan for the effective removal of one major lead source, housing stock, is presented.

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Ethanol self-administration in rats following exposure to dietary cadmium

Cited by 20 publications

References 26 publications

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

The future challenge of lead toxicity.

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