{"title":"The Significance of Intracellular Calcium in Rat Liver Cell Damage by Carbon Tetrachloride","authors":"H. Kröner , M. Planker","doi":"10.1016/S0005-8165(77)80050-4","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p>Early after intraperitoneal injection of carbon tetrachloride there is an influx of calcium into the liver cell (<span>Reynolds, 1963</span>; <span>Rees, 1962</span>). A previous study (<span>Kröner, 1973</span>) showed that increased intracellular calcium level is correlating with the loosing of cytoplasmatic enzymes. On the other hand Minot (1929) and Cantarow (1938) described a protective effect of calcium against the toxic manifestation of carbon tetrachloride poisoning. Varying the rat calcium uptake by giving vitamin D<sub>3</sub> or calcium gluconate we studied the influence of calcium on the release of enzymes and electrolyte shift in the early phase of liver cell injury.</p></div><div><h3>Material and Methods</h3><p>Experiments were performed with female Wistar rats, weighing 160–220 g and maintained on Altromin standard diet and water ad libitum. The rats were killed 2, 4 and 6 hours after intraperitoneal injection of carbon tetrachloride (1 ml/kg body weight). Calcium and magnesium were determined in serum and liver by atomic absorption spectrophotometry. Potassium and sodium were estimated by flame photometry. The activity of alanine-transaminase and lactate-dehydrogenase in serum was determined spectrophotometrically (Biochemica Test Combination, Boehringer Mannheim GmbH). Vitamin D<sub>3</sub> (Bayer/Merck) diluted in olive oil was applied by stomach tube 72 hours before experiments were started. Calcium gluconate solution was given simultaneously with carbon tetrachloride intraperitoneal.</p></div><div><h3>Results and Discussion</h3><p>The early rise of liver calcium after application of carbon tetrachloride was much larger in animals treated additionally with calcium gluconate or pretreated with vitamin D<sub>3</sub>. In contrast there were no distinct differences in plasma calcium. The additional treatment further caused a lesser resp. later shift of sodium and potassium in liver and an inhibition of enzyme release. The effects are specific for carbon tetrachloride poisoning. Analysis of intracellular distribution of calcium led us to the assumption of two different phenomena for the biphasic increase of calcium in liver described by Reynolds (1964) in carbon tetrachloride poisoning.</p></div>","PeriodicalId":75583,"journal":{"name":"Beitrage zur Pathologie","volume":"160 3","pages":"Pages 245-259"},"PeriodicalIF":0.0000,"publicationDate":"1977-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0005-8165(77)80050-4","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Beitrage zur Pathologie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0005816577800504","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 10
Abstract
Introduction
Early after intraperitoneal injection of carbon tetrachloride there is an influx of calcium into the liver cell (Reynolds, 1963; Rees, 1962). A previous study (Kröner, 1973) showed that increased intracellular calcium level is correlating with the loosing of cytoplasmatic enzymes. On the other hand Minot (1929) and Cantarow (1938) described a protective effect of calcium against the toxic manifestation of carbon tetrachloride poisoning. Varying the rat calcium uptake by giving vitamin D3 or calcium gluconate we studied the influence of calcium on the release of enzymes and electrolyte shift in the early phase of liver cell injury.
Material and Methods
Experiments were performed with female Wistar rats, weighing 160–220 g and maintained on Altromin standard diet and water ad libitum. The rats were killed 2, 4 and 6 hours after intraperitoneal injection of carbon tetrachloride (1 ml/kg body weight). Calcium and magnesium were determined in serum and liver by atomic absorption spectrophotometry. Potassium and sodium were estimated by flame photometry. The activity of alanine-transaminase and lactate-dehydrogenase in serum was determined spectrophotometrically (Biochemica Test Combination, Boehringer Mannheim GmbH). Vitamin D3 (Bayer/Merck) diluted in olive oil was applied by stomach tube 72 hours before experiments were started. Calcium gluconate solution was given simultaneously with carbon tetrachloride intraperitoneal.
Results and Discussion
The early rise of liver calcium after application of carbon tetrachloride was much larger in animals treated additionally with calcium gluconate or pretreated with vitamin D3. In contrast there were no distinct differences in plasma calcium. The additional treatment further caused a lesser resp. later shift of sodium and potassium in liver and an inhibition of enzyme release. The effects are specific for carbon tetrachloride poisoning. Analysis of intracellular distribution of calcium led us to the assumption of two different phenomena for the biphasic increase of calcium in liver described by Reynolds (1964) in carbon tetrachloride poisoning.
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