Protective effect of phenobarbital on cadmium toxicity in mice

1975 ◽  
Vol 34 (3) ◽  
pp. 517-520 ◽  
Author(s):  
Hiroshi Yoshikawa ◽  
Motoyasu Ohsawa
Keyword(s):  
Protective Effect ◽  
Cadmium Toxicity

scholarly journals Protective Effect of Edible Bird’s Nest on Ovaries of Cycling Female Rats Subjected to Cadmium Toxicity

2021 ◽  
Vol 9 (4) ◽  
Author(s):  
Abdul Quddus ◽  
Nurhusien Yimer ◽  
Faez Firdaus Abdullah Jesse ◽  
M. Mustapha Noordin ◽  
Mark W. H. Hiew ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cadmium Toxicity ◽  
Female Rats ◽  
Edible Bird’S Nest

scholarly journals Quercetin Protects Human Thyroid Cells against Cadmium Toxicity

2021 ◽  
Vol 22 (13) ◽  
pp. 6849
Author(s):  
Francesca Capriglione ◽  
Jessica Maiuolo ◽  
Marilena Celano ◽  
Giuseppe Damante ◽  
Diego Russo ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cadmium Toxicity ◽  
Human Thyroid ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Thyroid Cells ◽  
Ic50 Value ◽  
Mda Content ◽  
Molecular Effects ◽  
First Time

Various natural compounds have been successfully tested for preventing or counteracting the toxic effects of exposure to heavy metals. In this study, we analyzed the effects of cadmium chloride (CdCl2) on immortalized, non-tumorigenic thyroid cells Nthy-ori-3-1. We investigated the molecular mechanism underlying its toxic action as well as the potential protective effect of quercetin against CdCl2-induced damage. CdCl2 suppressed cell growth in a dose- and time-dependent manner (IC50 value ~10 µM) associated with a decrease in levels of phospho-ERK. In addition, CdCl2 elicited an increase in reactive oxygen species (ROS) production and lipid peroxidation. A significant increase in GRP78, an endoplasmic reticulum (ER) stress-related protein, was also observed. Supplementation of quercetin counteracted the growth-inhibiting action of CdCl2 by recovering ERK protein phosphorylation levels, attenuating ROS overproduction, decreasing MDA content and reducing the expression of GRP78 in cells exposed to CdCl2. Thus, in addition to revealing the molecular effects involved in cadmium-induced toxicity, the present study demonstrated, for the first time, a protective effect of quercetin against cadmium-induced damages to normal thyroid cells.

scholarly journals Protective effect of metallothionein on cadmium toxicity in isolated rat hepatocytes

1985 ◽  
Vol 230 (2) ◽  
pp. 395-402 ◽  
Author(s):  
W S Din ◽  
J M Frazier
Keyword(s):  
Protective Effect ◽  
Cadmium Toxicity ◽  
Membrane Damage ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Rat Hepatocytes ◽  
Detoxification Mechanism ◽  
Isolated Rat

An isolated rat hepatocyte preparation was used to study the cellular toxicity of cadmium and the protective effects of metallothionein on cadmium-induced toxicity. Exposure of primary suspension cultures of isolated rat hepatocytes to Cd2+ (0-35.7 microM) for 15 min resulted in a dose-dependent reduction in the synthesis of cellular proteins during a subsequent 6 h incubation. Such inhibition could not be correlated with cellular lethality or gross membrane damage. Pre-induction of metallothionein in hepatocytes by zinc treatment in vivo of donor rats protected hepatocytes in vitro from cadmium-induced inhibition of protein synthesis. The protective effects in zinc-pre-induced hepatocytes are not due to alterations in the level of total cellular cadmium, but could be accounted for by the redistribution of intracellular cadmium in the presence of high levels of zinc-metallothionein. The data suggest that metallothionein exerts its protective effect by a kinetic detoxification mechanism, i.e. a decrease in reactive intracellular cadmium.

Exogenous Nitric Oxide Reduces Cadmium Toxicity of Maize Roots

2011 ◽  
Vol 378-379 ◽  
pp. 409-413
Author(s):  
Hai Yan Li ◽  
Hong Shao
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Cadmium Toxicity ◽  
Maize Seedlings ◽  
No Donor ◽  
Cd Toxicity ◽  
Maize Roots ◽  
Exogenous Nitric Oxide ◽  
Enzymic Antioxidants

The effects of nitric oxide (NO) in protecting maize (Zea mays) roots against cadmium (Cd) toxicity were investigated. Maize seedlings pretreated for 24 h with 10-40 µM sodium nitroprusside (SNP), an NO donor, and subsequently exposed to 5 µM Cd for 24 h exhibited significantly greater root elongation as compared with the plants without SNP pretreatment. The pretreatment with 20 µM SNP alleviated Cd toxicity most obviously. SNP reduced Cd-induced accumulation of hydrogen peroxide (H2O2) and malonodialdehyde (MDA), which indicated NO alleviated Cd-induced oxidative damage. Cd treatment resulted in an upregulation of activities of superoxide dismutase (SOD), peroxidase (POD) and ascorbate peroxidase (APX) and the contents of glutathione (GSH) and ascorbate (ASC). Though SNP suppresses activities of POD, SOD and APX, it increases the production of non-enzymic antioxidants including glutathione (GSH) and ascorbate (ASC). The protective effect of SNP on Cd toxicity can be reversed by 2-(4-carboxy-2-phenyl)-4,4,5,5 -tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a NO scavenger, suggesting that the protective effect of SNP is attributable to NO released. These results suggest that NO plays an important role in protecting the plant against Cd-induced oxidative damage.

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