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Semethylselenocysteine, unlike selenomethionine, is not incorporated into proteins but may be converted directly to methylselenol by lyase. In one study, people from the regions with a high incidence of hepatocellular carcinoma; the other had their salt unfortied.The prostate cancer incidence decreased by a striking. Clinical cancer prevention trials demonstrate the potential strategy for reducing the burden of cancer on society.Phase I enzymes are members of the cytochrome P system responsible for converting chemical carcinogens to reactive adducts that can attack to DNA.On the other hand, defense against carcinogenic injury is provided by phase II detoxifying enzymes.This mechanism has been well documented to be important for the chemopreventive activity of many thiolreactive chemopreventive agents, mainly by inhibition of the initiation stage of carcinogenesis. Se was found to be a component of antioxidant defenses either as agent able to scavenge free radicals, or as a component of a family selenoenzymes.Se is found to be a component of several other selenoproteins, some of which have important enzymatic functions associated with antioxidant defenses.Additionally, iodothyronine deiodinase, produces the active thyroid hormone, T from an inactive precursor T.Another selenoprotein, selenoprotein P appears to protect endothelial cells against damage from free radicals. There was not unambiguous evidence supporting the role of any known selenoprotein in cancer prevention.Whether the selenoproteins are crucial to the anticancer effects needs to be elucidated.The functions of many of the human selenoproteins are as yet unknown, although some of them are involved in antioxidant and anabolic processes. Which of these effects elicited by the supranutritional andor toxic L.This hypothesis is based on the ability of all selenides. Exposure of cells to free radicals damages structure and consequently interferes with the functions of enzymes, nucleic acids and critical macromolecules.Selenotrisuldes are relatively stable, however, they can be reduced by excess thiols or by cellular glutathione reductase, forming a highly reactive selenopersulde anion. Although O has relatively low reactivity and toxicity, it gives rise to secondary oxidative products.Accordingly, DNA damaging activity of selenomethionine have recently been demonstrated in prostate cells of dogs fed by high doses. Previous studies have suggested that DNA damage is involved in the induction of events leading to apoptotic death in tumor cells. The methylselenide anion must be formed from these selenoamino acids in vivo by metabolic enzymes, methioninase. Data accumulated over many years clearly shows that oxidative DNA damage plays an important role in a number of disease processes, including malignant transformations. The major pathway eliminating DNA base damage, base free sites and SSB is excision repair, subdivided into nucleotide excision repair pathway and DSB by homologous recombination. Nevertheless, besides {|purchase {Endurobol|Amiodarone agents that induce exclusively different types of DNA damage, either directly or indirectly via intermediates, there are some agents which can also interfere with the repair of DNA thus increasing the adverse consequences of DNA lesions.Well recognized examples are the carcinogenic metal compounds, such as nickel, cobalt, cadmium and arsenic which were shown to inhibit BER and NER repair pathways at low, seemingly noncytotoxic concentrations.Potential target molecules for metal ions are the zinc nger structures in DNA repair proteins, with each zinc nger protein sensitive towards a specic toxic metal ions.

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