Intracellular diagnostics: hunting for the mode of action of redox-modulating selenium compounds in selected model systems.

Redox-modulating compounds derived from natural sources, such as redox active secondary metabolites, are currently of considerable interest in the field of chemoprevention, drug and phytoprotectant development. Unfortunately, the exact and occasionally even selective activity of such products, and the underlying (bio-)chemical causes thereof, are often only poorly understood. A combination of the nematode- and yeast-based assays provides a powerful platform to investigate a possible biological activity of a new compound and also to explore the "redox link" which may exist between its activity on the one side and its chemistry on the other.

Selenium toxicity toward yeast as assessed by microarray analysis and deletion mutant library screen: a role for DNA repair.

Selenium (Se) is a trace element that is essential for human health as it takes part in many cellular processes. The cellular response to this compound elicits very diverse processes including DNA damage response and repair. Because an inorganic form of Se, sodium selenite (SeL), has often been a part of numerous studies and because this form of Se is used as a dietary supplement by the public, here, we elucidated mechanisms of SeL-induced toxicity in yeast Saccharomyces cerevisiae using a combination of systematic genetic and transcriptome analysis.

Investigations on the role of base excision repair and non-homologous end-joining pathways in sodium selenite-induced toxicity and mutagenicity in Saccharomyces cerevisiae.

Selenium (Se) belongs to nutrients that are essential for human health. Biological activity of this compound, however, mainly depends on its dose, with a potential of Se to induce detrimental effects at high doses. Although mechanisms lying behind detrimental effects of Se are poorly understood yet, they involve DNA damage induction.

Rad52 has a role in the repair of sodium selenite-induced DNA damage in Saccharomyces cerevisiae.

Selenium (Se) is a chemo-preventive agent that has been shown to have a protective role against cancer. The inorganic form of Se, sodium selenite (Na2SeO3), has frequently been included in various chemo-prevention studies, and this commercially available form of Se is used as dietary supplement by the public. Because high doses of this Se compound can be toxic, the underlying molecular mechanisms of sodium selenite toxicity need to be elucidated.

Toxicity and mutagenicity of selenium compounds in Saccharomyces cerevisiae.

Selenium (Se) is an essential trace element for humans, animals and some bacteria which is important for many cellular processes. Se's bio-activity is mainly influenced by its chemical form and dose. The use of Se supplements in the human diet emphasizes the need to establish both the beneficial and detrimental doses of each Se compound.

Selenium: from cancer prevention to DNA damage.

Selenium (Se) is a dietary essential trace element with important biological roles. Accumulating evidence indicates that Se compounds possess anticancer properties. Se is specifically incorporated into proteins in the form of selenocysteine and non-specifically incorporated as selenomethionine in place of methionine.

Relative contribution of homologous recombination and non-homologous end-joining to DNA double-strand break repair after oxidative stress in Saccharomyces cerevisiae.

Oxidative damage to DNA seems to be an important factor in developing many human diseases including cancer. It involves base and sugar damage, base-free sites, DNA-protein cross-links and DNA single-strand (SSB) and double-strand (DSB) breaks. Oxidative DSB can be formed in various ways such as their direct induction by the drug or their generation either through attempted and aborted repair of primary DNA lesions or through DNA replication-dependent conversion of SSB.