The Significance of Intracellular Calcium in Rat Liver Cell Damage by Carbon Tetrachloride

Beitrage zur Pathologie Pub Date : 1977-07-01 DOI:10.1016/S0005-8165(77)80050-4

H. Kröner , M. Planker

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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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细胞内钙在大鼠四氯化碳肝细胞损伤中的意义

腹膜内注射四氯化碳后早期会有钙流入肝细胞(Reynolds, 1963;里斯,1962)。先前的一项研究(Kröner, 1973)表明，细胞内钙水平升高与细胞质酶的疏松有关。另一方面，Minot(1929)和Cantarow(1938)描述了钙对四氯化碳中毒毒性表现的保护作用。通过给药维生素D3和葡萄糖酸钙来改变大鼠的钙摄取，我们研究了钙对肝细胞损伤早期酶释放和电解质转移的影响。材料与方法选用雌性Wistar大鼠，体重160 ~ 220 g，饲喂Altromin标准日粮和水。腹腔注射四氯化碳(1 ml/kg体重)2、4、6 h后处死大鼠。用原子吸收分光光度法测定血清和肝脏中的钙、镁。用火焰光度法测定钾和钠。用分光光度法测定血清中丙氨酸转氨酶和乳酸脱氢酶的活性(Biochemica Test Combination, Boehringer Mannheim GmbH)。在实验开始前72小时，胃管给予用橄榄油稀释的维生素D3(拜耳/默克)。葡萄糖酸钙溶液与四氯化碳同时腹腔注射。结果与讨论添加葡萄糖酸钙或维生素D3预处理的动物，在四氯化碳处理后肝钙的早期升高要大得多。相比之下，血浆钙含量无明显差异。额外的治疗进一步造成了更少的反应。肝内钠和钾的迟移和酶释放的抑制。这种影响是针对四氯化碳中毒的。对钙在细胞内分布的分析使我们对Reynolds(1964)在四氯化碳中毒中描述的肝脏中钙的两相增加有两种不同的假设。

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