Denitrase activity of Debaryomyces�hansenii reduces the oxidized compound 3‑nitrotyrosine in mice liver with colitis

Abstract

The oxidation of tyrosine to 3-nitrotyrosine is irreversible, and due to this characteristic, 3-nitrotyrosine is used as a marker for oxidative stress in a range of diverse chronic and degenerative diseases. It has been established that the yeast Debaryomyces hansenii (D. hansenii) can assimilate free 3-nitrotyrosine as unique source of nitrogen, and during saline stress, has a high denitrase activity to detoxify this compound in a reaction that involves the liberation of nitrogen dioxide from 3-nitrotyrosine. However, until now it has not been determined whether D. hansenii can detoxify protein-bound 3-nitrotyrosine such as nitrated proteins present in different chronic illnesses. TThe aim of the present study was to evaluate the denitrase activity of D. hansenii to reduce 3-nitrotyrosine from liver proteins of mice with colitis. Firstly, the levels of reactive oxygen species of liver tissue of colitic and control mice were measured by the reaction with the 2'7'-dichlorofluorescein diacetate. Denitrase activity of D. hansenii was evaluated by incubating cell extracts of the yeast with protein extracts from livers of mice with colitis. Following incubation, 3-nitrotyrosine was measured, and to corroborate that denitrase reaction had occurred, the production of nitrites was measured. In samples of liver tissue from mice with colitis, the maximum levels of reactive oxygen species were up to two times higher compared with the control livers. Following the incubation of colitic liver samples with cell extracts of D. hansenii, it was observed that 3-nitrotyrosine decreased to the basal concentration of control liver samples, and that the concentration of nitrites was increased. These results indicate that denitrase of D. hansenii extracts can effectively detoxify 3-nitrotyrosine bound to proteins and that the extracts could be used to decrease protein oxidation damage in chronic degenerative diseases.

Fuzhuan brick tea ameliorates hepatic steatosis and steatohepatitis through gut microbiota-derived aryl hydrocarbon receptor ligands in high-fat diet-induced obese mice

“…53 In addition, Debaryomyces_hansenii β-glucans can regulate the genetic expression of different pro-inflammatory cytokines such as IL-1β and TNF-α, which induce fatty liver disease. [53][54][55] However, until now it has not been determined whether Debaryomyces_hansenii is related to AhR activity or AhR ligand production in the regulation of hepatic steatosis and steatohe-patitis, although in this study Debaryomyces_hansenii was detected to contribute to a significant fraction of the tryptophan metabolism genes in the sequence. But there is no doubt that Debaryomyces_hansenii plays an important role in the recovery of hepatic steatosis and steatohepatitis.…”

“…53 The antioxidant capacity of Debaryomyces_hansenii , due to the detoxification of oxidized 3-detoxification bound to proteins, can decrease protein oxidation damage and alleviate inflammatory response in the liver through reverting oxidative stress in the endoplasmic reticulum and modifying mitochondrial function in metabolic dysfunction and chronic inflammation conditions. 54 Besides, the function of Debaryomyces_hansenii in maintaining normal microbiome ecology by recovering beneficial bacteria but avoiding opportunistic pathogens can decrease the passage of bacteria or endotoxins from the intestine to the liver, which in turn alleviates liver inflammation and hepatobiliary damage. 53 In addition, Debaryomyces_hansenii β-glucans can regulate the genetic expression of different pro-inflammatory cytokines such as IL-1β and TNF-α , which induce fatty liver disease.…”

Blood Levels of Glutamine and Nitrotyrosine in Patients with Chronic Viral Hepatitis

“…Effective detoxification of the 3-nitrotyrosine bound to proteins decreases protein oxidation damage in such disorders. 11 In addition, nitrotyrosine is considered a biomarker of nitrogen free radical species modified proteins. 12 The antioxidant therapy is not always effective as add-on treatment for hepatitis because antioxidants; if not used at the right setting and dosing schedule; they can become pro-oxidants.…”