Anatomical and Histological Study of the Effect of Lead on Hepatocytes of Albino Rats

Abstract

Lead is found at low levels in Earth's crust, mainly as lead sulfide. Lead is toxic for virtually all organs of the body and has significant debilitating effects on the nervous, renal, hepatic and hematopoietic systems. The liver is considered as one of the target organs affected by lead toxicity owing to its site of storage after exposure. Also, the liver is being one of the major organs involved in the biotransformation and detoxification of toxic substances. Absorbed lead is stored in soft tissues mainly in the liver via the portal vein, so that it is the first organ for which the histological analysis can be used to examine the morphological changes that reflect possible lead effects on somatic cells. The present study aimed to determine the structural damage in the liver by histological study and biochemical assay of liver enzyme levels. 45 rats were divided into 3 groups. Group I (control group) included 15 rats that were given distilled water by orogastric tube. Group II (experimental group) included 15 rats that were given lead acetate in a dose of 4mg/kg body weight by orogastric tube for two weeks. Group III (experimental group) included 15 rats given lead acetate by the same route and dose for four weeks. Significant increase of liver enzymes SGPT and SGOT was observed in experimental groups (group II and III). Administration of lead acetate for 2 weeks (group II) induced alteration in the hepatic architecture as evident by some of the hepatocytes appeared with acidophilic slightly vacuolated granular cytoplasm while others showed markedly vacuolated hypereosinophilic cytoplasm, Mononuclear cellular infiltration was seen in the portal tract. While in Group III, diffuse affection of the hepatic lobule was evident by extensive vacuolation of the hepatocyte cytoplasm, dark and eccentric nuclei. Others showed kayolytic nucleus, congested central vein, narrow or even obliterated blood sinusoids. The portal area revealed proliferation of bile ducts and congestion of its vessels. The hepatic architecture was disorganized with marked affection of the hepatocytes. In conclusion it was found that lead acetate is toxic to liver and this toxicity is paralleled with increased duration of exposure.

Study The Effects of Lead and Cadmium on The Kidney and Liver of Albino Rats

“…In this study, the male rats were treated with Pb, the histological sections demonstrated changes in the liver tissue such as congestion, necrosis, central vein dilation, liver vacuolation, inflammatory cell infiltration, and hyperplasia [12].…”

Pathomorphology of fetal and mature liver under the lead intoxication and after the correction: the review of experimental data

“…It was found that the main toxic effect of lead in the mature liver was the alteration of membranes of the endothelium, red blood cells and hepatocytes [12]. The typical morphological changes in the liver in experiments with short period lead treatment were the hypertrophy of hepatocytes, vacuolization of cytoplasm, portal space and central vein dilatation, congested central veins, narrowing or even obliteration of sinusoids and the activation of macrophages and lymphocytes with further mononuclear cellular infiltration of the portal tracts [11,26]. The degree of the liver alteration was dependent on the duration of lead exposure [11].…”

“…The typical morphological changes in the liver in experiments with short period lead treatment were the hypertrophy of hepatocytes, vacuolization of cytoplasm, portal space and central vein dilatation, congested central veins, narrowing or even obliteration of sinusoids and the activation of macrophages and lymphocytes with further mononuclear cellular infiltration of the portal tracts [11,26]. The degree of the liver alteration was dependent on the duration of lead exposure [11]. The submicroscopic changes of hepatocytes included the alteration of mitochondria, nuclei and membranes of hepatocytes.…”

“…There were signs of cytolysis, karyolysis, dissociation of hepatocytes, hyperplasia of mitochondria, swelling of their matrix, dissociation and disappearance of the mitochondrial crists. The terminal disturbance in hepatocytes differentiation was the lack of their polyploidization [11].…”