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

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.

Evaluation of several novel alkynols, alkenols, and selected host odor blends as attractants to female Aedes albopictus and Culex quinquefasciatus.

The compound 1-octen-3-ol is a strong attractant for some mosquito species. Based on chemical structure, this may be due to a terminal site of unsaturation or high electron density, a structural capability for hydrogen bonding, e.g.

Semi-field evaluation of several novel alkenol analogs of 1-octen-3-ol as attractants to adult Aedes albopictus and Culex quinquefasciatus.

The compound 1-octen-3-ol is a known attractant of some mosquito species, which has led to the hypothesis that olfactory stimulation by this alkenol may be associated with the following structural elements: a terminal site of unsaturation or high electron density; a structural capability for hydrogen bonding, e.g., -OH, -NH2, NHR, NR2, etc.

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

Cadmium is non-essential, carcinogenic and multitarget pollutant in the environment. Monoisoamyl-2,3-dimercaptosuccinate (MiADMS) is an ester of dimercaptosuccinic acid that acts as an antioxidant and chelator. Therefore, the mitigative action of MiADMS on viability, morphology, antioxidative enzymes and cell cycle were studied on rat liver cells treated with cadmium chloride (CdCl2).

Protective effects of N-acetylcysteine against cadmium-induced damage in cultured rat normal liver cells.

In this study, the protective effects of N-acetylcysteine (NAC), a precursor of reduced glutathione, were studied by measuring the viability, the levels of antioxidant enzymes, and by analyzing the cell cycle in cadmium (Cd)-treated rat liver cells. The cells were treated with 150 µM CdCl2 alone or co-treated with 150 µM CdCl2 and 5 mM NAC (2 h pre-, simultaneous or 2 h post-treatment) for 24 h. The viability of the cells treated with 150 µM CdCl2 alone decreased to 40.