Mitigative action of monoisoamyl-2,3-dimercaptosuccinate (MiADMS) against cadmium-induced damage in cultured rat normal liver cells

Environmental Toxicology

Fils-Aime

Badisa

et al. 2014

Self Cite

Cadmium is commercially profitable element, but it causes toxicity in humans and animals leading to diseases in various organs. The main route of cadmium exposure to humans is through inhalation. Lungs respond to insult through secretion of cytokines. In this study, the chemo-protective effect of monoisoamyl 2, 3-dimercaptosuccinate (MiADMS) was evaluated on viability and cytokines expression in CdCl2 treated human lung A549 cells by cytokine array. Cells were treated with 0, 50, 75 and 100 μM CdCl2 alone, 300 μM MiADMS alone, and co-treated with 300 μM MiADMS and 75 μM CdCl2 for 24 h. The viability was measured by crystal violet dye. The level of cytokines in the cells’ lysate and cell culture medium was measured using Ray Biotech's Human Cytokine Array 6 in control cells, 75 μM CdCl2 alone and MiADMS co-treated cells. Array results were validated by ELISA kit. The CdCl2 caused a dose dependent decrease in cell viability, while MiADMS co-treatment resulted in a significant increase in viability of CdCl2 treated cells. Morphology of the cells treated with CdCl2 was destroyed, while MiADMS restored the lost shape in CdCl2 treated cells. In addition, the cells co-treated with MiADMS and CdCl2 showed modulation of cytokines expression in comparison to the CdCl2 alone treated cells. The ELISA results showed the similar pattern of cytokine expression as Human Cytokine Array and validated the array results. These results clearly show the chemo-protective effect of MiADMS and suggest that MiADMS can be used as antidote at moderate dose against CdCl2 toxicity.

Section: Discussionmentioning

confidence: 99%

Chemoprotective effect of monoisoamyl 2, 3‐dimercaptosuccinate (MiADMS) on cytokines expression in cadmium chloride treated human lung cells

Environmental Toxicology

Fils-Aime

Badisa

et al. 2014

Self Cite

“…Our previous study investigated cadmium toxicity and the protective effect of different antioxidant or chelating compounds, which reduce the toxic effect of cadmium in liver cells (12)(13)(14)(15). Inhalation is one of the predominant causes of cadmium exposure in humans and it has been reported to cause chronic inflammation and is responsible for various lung diseases (16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Effect of cadmium on the expression levels of interleukin-1α and interleukin-10 cytokines in human lung cells

Molecular Medicine Reports

Latinwo

Sinclair

et al. 2015

Self Cite

Cadmium is an environmentally hazardous metal, which causes toxicity in humans. Inhalation of cigarette smoke and industrial fumes containing cadmium are sources of cadmium exposure. It is responsible for the malfunction of various organs, leading to disease particularly in the lungs, liver and kidneys. In the present study, the effect of cadmium chloride (CdCl2) on cell viability, and the expression levels of interleukin (IL)-1α and IL-10 cytokines at various concentrations and incubation durations were assessed in MRC-9 human normal lung and A549 human lung cancer cells to elucidate the mechanism of cadmium toxicity. Cell viability was measured using a crystal violet dye binding assay. The expression levels of the cytokines were measured by cytokine specific enzyme-linked immunosorbent assay kits. The viability assay results revealed higher sensitivity of the A549 lung cancer cells to CdCl2 compared with the normal MRC-9 lung cells. In the normal MRC-9 lung cells, higher expression levels of the cytokines were observed at the lowest CdCl2 concentration at a shorter exposure time compared with the lung cancer cells. Higher levels of the cytokines were observed in the A549 lung cancer cells at all other times and concentrations compared with the MRC-9 cells, indicating higher levels of inflammation. The cytokine levels were reduced at higher CdCl2 concentrations and longer exposure durations, demonstrating the toxic effect of cadmium. The results indicated that CdCl2 affected the expression levels of the cytokines and led to cytotoxicity in human lung cells, and suggested that compounds which reduce inflammation may prevent cadmium toxicity.

“…CdCl 2 toxicity at various concentrations in animal models and cell lines has been studied. In our previous reports, we studied the ameliorative effects of N ‐acetyl cysteine and MiADMS compounds on anti‐oxidant enzymes status in 150 μM CdCl 2 treated liver CRL 1439 cell line . Besides our studies, high dose of 100 μM Cd was used to induce cytotoxicity which led to 30% and 50% mortality after 24 and 48 hours treatment, respectively, in keratinocyte cell line, and lethal dose of 350 μM was used to study apoptosis in lymphoblastoid cell line .…”

Section: Discussionmentioning

confidence: 91%

“…Antagonist or protective compounds have been used to reduce the toxic effects of Cd in various cell lines or animal models . In this report, the protective effect of DADS against Cd‐induced toxicity was evaluated.…”

Section: Resultsmentioning

confidence: 99%

“…Many isolated compounds or plant extracts that possess anti‐oxidant properties have been evaluated in reducing environmental Cd‐induced damage in various organs . Thiol (sulfhydryl groups) containing compounds which function as metal chelators also have been tested to ameliorate the effects of metals in cell lines or animal models . Garlic, which possesses sulfhydryl compounds, is a plant product that has been used as a protective agent for various human disorders.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Diallyl disulfide attenuation effect on transcriptome in rat liver cells against cadmium chloride toxicity

Ahkinyala

Lyles

Environmental Toxicology

et al. 2019

In this report, liver cells were treated with cadmium chloride (CdCl 2 ) and diallyl disulfide (DADS), a major compound from garlic to attenuate the toxic effect of Cd on transcriptome. The viability of Cd treated cells was reduced to 19.9% ± 2.4% in comparison to the untreated cells, whereas the viability of DADS pretreated cells was increased to 48.6% ± 2%. The attenuation effect of DADS was studied at shorter period (6 hours). Transcriptome analysis of CdCl 2 alone treated cells resulted in 2119 and 982 (up and down) regulated genes (≥ 2 or ≤ 2-fold), whereas pretreated cells with DADS resulted in 2597 and 1784 genes. These genes were known to function in many important biological processes. Affymetrix array analysis was validated by the pathway specific PCR array that exhibited the same trend of expression. The current study clearly shows the DADS attenuation effect on transcriptome in CdCl 2treated rat liver cells. K E Y W O R D S cadmium chloride, cell cycle, diallyl disulfide, GeneAtlas, transcriptome