Cadmium-Induced Liver, Heart, and Spleen Lipid Peroxidation in Rats and Protection by Selenium

Yiin, Shuenn-Jiun; Chern, Chi-Liang; Sheu, Jenn-Yuan; Lin, Te-Hsien

doi:10.1385/bter:78:1-3:219

Cited by 65 publications

(44 citation statements)

References 29 publications

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“…The elevation in the creatinine was presumably due to nephrotoxic effect of Cd on renal tubules and glomeruli (Abdo and Abdulla, 2013). In support of these findings, it was reported that long-term Cd exposure causes depletion of liver and muscular glycogen, due to its action on the enzymes involved in glycogenesis and energy metabolism (Toury et al, 1985) and induces oxidative stress in the liver and kidney (Yiin et al, 1999). Our results…”

supporting

confidence: 91%

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

Abou-Kassem

Mahrose

Alagawany

2016

Animal

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This study was conducted to verify whether vitamin (Vit) E or natural clay as feed additives has the potential to modulate the deleterious effects resulting from exposure to cadmium (Cd) in growing Japanese quail. 648 Japanese quail chicks (1 week old) were used to evaluate the effects of dietary Cd (0, 40, 80 and 120 mg/kg diet) and two levels of Vit E (0, 250 mg/kg diet) or two levels of natural clay (0 and 100 mg/kg diet) to study the influences of Cd, Vit E, clay or their different combinations on growth performance, carcass traits, some blood biochemical components and Cd residues in muscles and liver. Live BW and weight gain of quails were linearly decreased with increasing dietary Cd levels. Moreover, feed conversion was significantly worsened with increasing Cd level. Mortality percentage was linearly increased as dietary Cd level increased up to 120 mg/kg diet. Carcass percentage was linearly decreased as dietary Cd level increased. While, giblets percentage were linearly and quadratically differed as dietary Cd level increased. Cd caused significant changes in total plasma protein, albumin, globulin, A/G ratio, creatinine, urea-N and uric acid concentrations as well as ALT, AST and ALP activities. Increasing dietary Cd level was associated with its increase in the muscles and liver. Dietary supplementation with 250 mg of Vit E/kg diet or 100 mg clay/kg improved live BW, BW gain and feed conversion when compared with the un-supplemented diet. Quails fed diet contained 250 mg Vit E/kg and those fed 100 mg clay/kg had the highest percentages of carcass and dressing than those fed the un-supplemented diet. Blood plasma biochemical components studied were better when birds received 250 mg of Vit E/kg diet and those received 100 mg clay/kg. Cd residues in the muscles and liver were significantly less in the birds had 250 mg of Vit E/kg or those received 100 mg clay/kg diet than those un-supplemented with Vit E. Growth performance traits and blood plasma biochemical components studied were significantly affected linearly by the interactions among Cd and each of Vit E and clay levels. In conclusion, the present results indicate that the deleterious effects induced by Cd plays a role in decreasing the performance of Japanese quail and that dietary supplementation with natural clay or Vit E may be useful in partly alleviating the adverse effects of Cd.

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supporting

confidence: 91%

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

Abou-Kassem

Mahrose

Alagawany

2016

Animal

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“…Oxidative stress is one of the mechanisms that contribute to structural changes or misfolding of proteins such as SOD. Lipid peroxidation has been considered as the primary mechanism for cadmium toxicity [Muller, 1986;Yiin et al, 1990;Manca et al, 1999]. It has been proposed that the enhancement of lipid peroxidation by cadmium in rats is a consequence of a decrease in superoxide dismutase and catalase activity [Hussain et al, 1987;Shukla et al, 1989;Stajn et al, 1997].…”

Section: Discussionmentioning

confidence: 99%

Effects of cadmium on structure and enzymatic activity of Cu,Zn‐SOD and oxidative status in neural cells

Huang

Shih

Huang

et al. 2006

J of Cellular Biochemistry

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder disease. Ten percent of the ALS patients are congenital (familial ALS), and the other 90% are sporadic ALS (SALS). It has been shown that mutations found in the Cu,Zn-SOD cause 20% of the familial ALS due to its low enzyme activity. We hypothesized that heavy metals may interfere the structure of Cu,Zn-SOD protein to suppress its activity in some of the SALS. In this study, we expressed and characterized the recombinant human Cu,Zn-SOD under various concentrations of Cu . By atomic absorption spectrophotometry, we demonstrated that adding of cadmium significantly increased the content of cadmium ion, but reduced its Zn 2þ content and enzyme activity of the Cu,Zn-SOD protein. The data of circular dichroism spectra demonstrated that the secondary structure of Cu,Zn-SOD/Cd is different from Cu,Zn-SOD, but close to apo-SOD. In addition to the effect of cadmium on Cu,Zn-SOD, cadmium was also shown to induce neural cell apoptosis. To further investigate the mechanism of neural cell apoptosis induced by cadmium, we used proteomics to analyze the altered protein expressions in neural cells treated with cadmium. The altered proteins include cellular structural proteins, stressrelated and chaperone proteins, proteins involved in reactive oxygen species (ROS), enzyme proteins, and proteins that mediated cell death and survival signaling. Taken together, in this paper, we demonstrate that cadmium decreases the content of Zn 2þ , changes the conformation of Cu,Zn-SOD protein to decrease its enzyme activity, and causes oxidative stress-induced neural cell apoptosis.

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“…For the general population that is mainly exposed by oral and inhalation routes, Kidneys (mainly renal cortex) and liver are considered to be the most susceptible organs in the case of exposure to cadmium [18][19][20] . The soluble salts of Cadmium accumulate in the organism and affect toxically not only the liver and kidneys, but also the brain, lungs, testicles, central nervous system and other tissues [21] .…”

Section: Introductionmentioning

confidence: 99%

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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Cadmium-Induced Liver, Heart, and Spleen Lipid Peroxidation in Rats and Protection by Selenium

Cited by 65 publications

References 29 publications

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

Effects of cadmium on structure and enzymatic activity of Cu,Zn‐SOD and oxidative status in neural cells

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

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