Cadmium chloride

About: Cadmium chloride is a research topic. Over the lifetime, 3060 publications have been published within this topic receiving 63113 citations. The topic is also known as: CdCl2 & [CdCl2].

Immunosuppression produced by lead, cadmium, and mercury.

Abstract: Rabbits given lead acetate, cadmium chloride, or mercuric chloride in their drinking water for 70 days and then inoculated with pseudorabies virus (3 doses, 7 days between doses) as antigen had significantly lower neutralizing antibody titers than did the controls. The titers were determined by the plaque assay method using serum samples prepared 7 (experimental day 78) and 24 (experimental day 95) days after the first viral innoculation was given.

Assessment of cytotoxicity using electric cell-substrate impedance sensing: concentration and time response function approach.

Abstract: This paper describes a simple and convenient method to measure the concentration and time response function f (C,t) of cells exposed to a toxicant by electric cell−substrate impedance sensing. Attachment and spreading of fibroblastic V79 cells cultured on small gold electrodes precoated with fibronectin were detected as electrical resistance changes. With this method, chemical cytotoxicity was easily screened by observing the response function of attached cells in the presence of inhibitor. The cytotoxicities of three test models, cadmium chloride, sodium arsenate, and benzalkonium chloride, were quantified by measuring the percentage inhibition as a function of the inhibitor concentration. The half-inhibition concentration, the required concentration to achieve 50% inhibition, derived from the response function agreed well with the results obtained using the standard neutral red assay.

Is the capacity of lead acetate and cadmium chloride to induce genotoxic damage due to direct DNA–metal interaction?

Abstract: Even though the toxic effects of lead and cadmium compounds have been studied over many years, inconsistent results have been obtained about their mutagenic, clastogenic and carcinogenic properties. However, these metals are considered to be potential human carcinogens. The mechanism of metal-induced carcinogenesis is still unknown, but one possible pathway may involve the interaction of metals with DNA, either directly or indirectly. In this work we explore the capacity of lead, cadmium or a mixture of both metals to interact with acellular DNA, by employing a variant of the comet assay. Our results, using low non-cytotoxic metal concentrations (0.01, 0.1 and 1.0 microM) with the standard protocol for the acellular assay, showed an induction of DNA damage in cells of all organs studied; however, basal DNA damage was different in each organ. To confirm that we were working with pure DNA, proteinase K was added to the lysis solution. With this enriched-lysis solution we found a negative response in the induction of DNA damage in cells derived from the liver, kidney and lung of CD-1 male mice. To support the results obtained by the enriched-acellular assay, we studied the capacity of lead and cadmium (0.1 microM) to induce breaks in pooled genomic DNA in cells of the same organs, with negative results. Consistent with these findings, these metals do not induce DNA breaks in the plasmid pUSE amp+. On the whole, we did not detect direct induction of DNA strand breaks by lead acetate, cadmium chloride or a mixture of both metals, all at low non-cytotoxic concentrations. However, we found an induction of lipid peroxidation and an increase in free radical levels in the different organs of CD-1 male mice after inhalation of lead acetate (0.0068 microg/cc) or cadmium chloride (0.08 microg/cc) for 1 h, suggesting the induction of genotoxicity and carcinogenicity by indirect interactions, such as oxidative stress.