Effect of Zinc on Lead Acetate Induced Liver and Stomach Injury in Adult Mice: Electron microscopic and Biochemical Study

Background: Lead is one of the common heavy metals to which people are exposed daily. It is found in drinking water, and occurs naturally in soil but at low levels in Earth’s crust, as lead sulfide. Lead is considered dangerous and can cause environmental pollution due to its toxic effects on livings. Gastrointestinal ingestion is the most common source of lead intake in the body. Chronic exposure to lead even in low doses can induce liver damage as it is considered as one of the target organs affected by lead toxicity. Zinc is an essential trace element, exerting a protective effect as anti-inflammatory, antiapoptotic and antioxidant but these hepatoprotective properties have not been fully elucidated.
Aim of the work: The present study was designed to detect the possible protective effect of Zinc against the toxic effects of lead acetate on liver and stomach of mice.
Material and Methods: Sixty healthy adult mice were randomly divided into 3 groups of 20 mice each. Group I (Control group) were given distilled water by orogastric tube. Group II (Experimental group) were given lead acetate in a dose of 4mg/kg body weight by orogastric tube for 2 weeks. Group III (Experimental group) were given lead acetate and Zinc in a dose of 25 mg/kg/body weight by orogastric tube for 2 weeks. After two weeks biochemical and electron microscopic examinations of the liver and stomach were done.
Results: Significant increase of liver enzymes SGPT and SGOT was observed in experimental groups (group II and III) but more increased in group II. Electron microscopic examination group II revealed marked changes involving both the cytoplasm and the nucleus. The cytoplasm showed many vacuoles, multiple lipid droplets, areas of necrosis, dilated rough endoplasmic reticulum, dilated smooth endoplasmic reticulum and pleomorphic mitochondria with dense matrix. The nuclei of most of the hepatocytes showed dilated perinuclear cisternae, variability in shape and size of nuclei was noticed with vesiculation of their chromatin content. Many abnormal Kupffer cells were seen lining the blood sinusoids, distorted bile canaliculi and areas of necrosis were seen. Electron microscopic examination of group III revealed moderate changes of most liver cells. The cytoplasm exhibited pleomorphic mitochondria with dense matrix, dilated rough endoplasmic reticulum and dilated smooth endoplasmic reticulum, many lysosomes and glycogen. The nuclei are binucleated and irregular. Stomach of mice group II revealed pocket in nucleus, dialysis of organelles and abnormal Golgi, the lumen with no microvilli and dark spots of lead in it, two cells with membrane in between irregular nucleus and lysis of rough endoplasmic reticulum and disturbed smooth endoplasmic reticulum. The stomach of mice group III revealed Nucleus with membrane slightly interrupted, the lumen with few microvilli, multiple secretory granules and disturbed rough Endoplasmic Reticulum.
Conclusion: Lead acetate induces chronic inflammation, oxidative stress and toxic injury in the liver and can change the structure of stomach mucosa. Zinc supplementation partially attenuated lead -induced liver and stomach injury as measured by biochemical, and electronmicroscopic studies and differences in structure has been observed between the Zinc and lead, lead and the control groups. Present study results demonstrate the protective effect of Zinc in decreasing but not a complete protective effect in lead induced significant toxic pathological changes in the liver and stomach of the albino mice.