Role of vitamin-E on rat liver-amiodarone: An ultrastructural study

Abstract

Background/Aim:Amiodarone, a class III antiarrhythmic drug, has been found to be effective in the management of patients with life-threatening ventricular arrhythmias. The aim of this study was to test whether the co administration of vitamin-E with amiodarone can reduce amiodarone-induced liver damage.Materials and Methods:Twelve male albino rats were divided into three groups (ml vegetable oil/day by oral gavages daily for 2 weeks and were used as control group. The rats of the second group received 5.4 mg amiodarone/100 gm rat dissolved in vegetable oil daily by oral gavages for 2 weeks. In the third group, the rats received 5.4 mg amiodarone and 5 mg vitamin-E/100 gram rat dissolved in 2 ml vegetable oil by oral gavages daily for 2 weeks. Two weeks after treatment, the rats were sacrificed and liver specimens were immediately taken and processed for transmission electron microscopic examinations.Results:Sections from the rat liver receiving amiodarone examined by electron microscopy showed disrupted hepatocytes with increased vacuolations. Degenerated organelles and disrupted nuclei were observed. The microvilli of bile canaliculi were disrupted and the hepatocytes showed increased lipid contents. Both endothelial cells and Kupffer cells were damaged. Phospholipids inside the mitochondria showed a loss of cristae. Sections from the liver of rats received amiodarone and vitamin-E showed lesser effects, especially in depositions of phospholipids in the mitochondria and the whole organelles and the nucleus showed minor damage in comparison to the previous group.Conclusion:Milder hepatotoxic effects are seen in rats administered amiodarone and vitamin E simultaneously suggesting that vitamin-E may play a role in amelioration of the effects of amiodarone.

Screening of herbal components for attenuating amiodarone-induced hepatotoxicity on gel-entrapped rat hepatocytes

“…Because vitamin E is the most potent protectant against AMD-induced liver injury in rats (Agoston et al, 2003), it was applied as a positive control in our investigation, which dramatically suppressed GSH depletion and lipid peroxidation (LPO), but showed little effect on lipid accumulation induced by AMD (Figure 2). The detected GSH retrieval and lipid reduction by vitamin E were all well in agreement with its antioxidant effects in vivo (Agoston et al, 2003;Zaki & Eid, 2009).…”

“…So far, only vitamin E, a lipophilic antioxidant, was proposed to potently attenuate AMD-induced toxicity in vivo (Agoston et al, 2003;Zaki & Eid, 2009) or in cultured hepatocytes (Ouazzani-Chahdi et al, 2007;Ruch et al, 1991). Such protection could be further enhanced by synergistic use of ursodeoxycholic acid or its nitric-oxidereleasing derivative, NCX-1000 (Ouazzani-Chahdi et al, 2007).…”

Vitamin E Ameliorates the Toxic Effect of Amiodarone on Thyroid Gland in Rats: A Histological and Ultrastructural Study

“…These findings were in agreement with Yu et al, (2011) who found that vitamin E may increase thyroid antioxidant defenses and inhibit iodine-induced thyroid cytotoxicity [37] . Also, Zaki, and Eid, (2009) who observed that α tocopherol could protect rat hepatocytes in culture from the damaging effect of amiodarone [20] . Murray et al (2000) reported that vitamin E protects against peroxidation of polyunsaturated fatty acids, which were part of cellular and subcellular membrane phospholipids [38] .…”

“…Cappiello et al (1995) suggested that amiodarone increases the permeability of the mitochondrial membrane with subsequent diffusion of glycogen synthesis enzymes that increase the intramitochondrial glycogen [36] . Also, Zaky and Eid, (2018) clarified that intramitochondrial accumulation of lipid droplets occurred due to inhibition of mitochondrial beta-oxidation by amiodarone therapy [20] .…”

“…Vitamin E has high affinity to phospholipids, cholesterol and triglycerides (the three main structural elements of the cell membrane, mitochondria and endoplasmic reticulum) thus vitamin E appears to be the first line of defense against peroxidation of the polyunsaturated fatty acids of the cell membrane [20] . It can break free radical chain reactions due to its ability to transfer phenolic hydrogen to peroxyl free radical of the cell membrane producing a stable non-radical product finally excreted in bile.…”