Mechanisms of cadmium-mediated acute hepatotoxicity

Rikans, Lora E.; Yamano, Tetsuo

doi:10.1002/(sici)1099-0461(2000)14:2<110::aid-jbt7>3.0.co;2-j

Cited by 376 publications

(225 citation statements)

References 70 publications

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“…These characteristic features of Cadmium-induced liver toxicity were similar to those previously reported by other investigators [62,63] . Several mechanisms have been suggested for the induction of Cadmium-associated hepatotoxicity [62] . The two enzymes ALT and AST are found in the liver and have been widely used for diagnostic purposes.…”

Section: Discussionsupporting

confidence: 90%

Camel's Milk Protects Against Cadmium Chloride Induced Toxicity in White Albino Rats

Al‐Hashem¹,

Dallak²,

Bashir³

et al. 2009

American J. of Pharmacology and Toxicology

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Problem statement:Cadmium is one of the most dangerous occupational and environmental toxins. It is found in drinking water, atmospheric air and even in food. Cadmium is reported to be very toxic to biological systems. Until now in treating intoxication with this metal, chelating Compounds have been used, burdened with numerous undesirable symptoms. For this reason, many researches are carried out in many countries to find natural-made compounds that help in the protection against cadmium induced toxicity with fewer or no side effects. This study was conducted to demonstrate the effect of daily oral Camel's milk administration against Cadmium chloride induced toxicity in white albino rats. Approach: White albino rats of both sexes (230-250 g) were housed in standard metal cages (6 rats/cage). The experimental rats (6 in each group) distributed into two experimental groups with a shared control group received only normal saline orally (Group 1). In experimental first group a daily dose (10 mg kg  1 body weight) of cadmium chloride was orally administrated to the rats for 21 days and named Cadmium chloride treated rats. In experimental second group, the same concentrations of cadmium chloride was dissolved in 2 mL of early morning fresh Camel's milk and the whole solution was administered into the experimental rats for 21 days and named Camel's milk cadmium chloride treated group. Water and food were provided ad libitum. Results: The data indicated that, in experimental Cadmium chloride treated rats, serum albumin, calcium and blood hemoglobin were decreased compared with control group received normal saline only. Moreover, Camel's milk administration with cadmium chloride showed a significant improvement of albumin, hemoglobin and calcium levels in the serum of the rats compared with cadmium chloride treated rats. Serum iron, sodium, chloride and urea levels were significantly increased in cadmium chloride treated rats compared with control group, while the addition of camel's milk to cadmium chloride decreased the high levels of these serum parameters in the treated rats. The enzyme activities of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and serum Alkaline Phaospatase (ALP) were significantly increased by orally administration of cadmium chloride compared with control group, while adding Camel's milk to cadmium chloride decreased the high levels of these enzymes comparing with the cadmium chloride treated rats. Cadmium chloride administration resulted in a high concentration of lipid peroxidation markers; TBARS and Hydroperoxides in comparison to control group, adding camel's milk to the cadmium chloride restored the levels of these markers to their normal levels in comparing to Cadmium chloride treated rats. Also treatment with cadmium chloride alone caused a significant decrease in both the enzymatic and nonenzymatic markers of oxidative stress (superoxide dismutase and catalase) and reduced glutathione, respectively in the liver tissues of treated rats, while the admini...

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Section: Discussionsupporting

confidence: 90%

Camel's Milk Protects Against Cadmium Chloride Induced Toxicity in White Albino Rats

Al‐Hashem¹,

Dallak²,

Bashir³

et al. 2009

American J. of Pharmacology and Toxicology

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“…Moreover, TNF-α and IL-1β are recognized to stimulate the production of adhesion molecules, such as intercellular adhesion molecule-1 (IMAC-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, P-selectin, β 2 -integrin Mac-1 in the liver, that induce the recruitment, adherence and activation of circulating inflammatory cells [31]. Rikans and Yamano [32], suggested that the hepatic endothelial cells might be the first cellular target for Cd-induced hepatocellular injury. Cdinduced degeneration of the hepatic endothelium is indicated by the extrusion of damage cells into the capillary lumen, producing a local ischemia in the parenchyma.…”

Section: Involvement Of Inflammatory Mediators and Adhesion Moleculesmentioning

confidence: 99%

“…The importance of sulfhydryl group reactions to Cd-induced hepatotoxicity is in part, the protection provided by MT and GSH, compounds that are rich in cysteine residues [32]. The inactivation of protein and non-protein thiols might also produce toxicity by disrupting the intracellular redox state, which in turn, could affect a number of important biological processes.…”

Section: Sulfhydryl Group Inactivation and Oxidative Stressmentioning

confidence: 99%

Liver and Cadmium Toxicity

2013

J Drug Metab Toxicol

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“…In addition, loss of bone calcium induced by long-term cadmium exposure results in bone injury consisting of a combination of osteomalacia and osteoporosis, which is called Itai-Itai disease. [66][67][68][69][70] Recently, there were many studies have shown that cadmium could accumulate in kidney, liver, lung and reproductive tissues in which the physiological functions were damaged. 69,[71][72][73] A previous study has shown that exposure of experimental animals to cadmium compounds (0.84 mg/kg) increased the blood glucose concentration.…”

Section: Cadmiummentioning

confidence: 99%

“…Cadmium-induced cellular toxicity has been described in various targets including metalloenzymes interference, thiol protein alterations, energy metabolism inhibition, DNA and membrane structure/function alterations, and excessive oxidative damage. 68,69,[76][77][78] Moreover, several studies have shown that cadmium-induced hyperglycemia was associated with increased lipid peroxidation, decreased insulin release, increased activation of gluconeogenic enzymes and impaired insulin receptor. 74,[78][79][80] Cadmium has also been demonstrated to induce a dose-dependent reduction in GLUT4 protein and mRNA expressions in rat adipocytes.…”

Section: Cadmiummentioning

confidence: 99%