Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: KEGG:D02003 (
NBT
)
1,323
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In recent years, it has been demonstrated that certain fatty acids are involved in the modulation of immune system functions. The mechanisms responsible for these effects are not fully elucidated, but many hypotheses have described numerous changes in the cell functionality as the main factors capable of altering the immune functions. In the present investigation, we have analysed the potential effects of FFA on cell viability, production of superoxide radicals or
proteasome
activity in assays in vitro. Thus, different FFA, such as OA, EPA or SA have been incorporated to cellular cultures at a concentration of 100 microM. Phospholipase, cyclooxygenase or lipooxygenase inhibitors abolished the loss of thymocyte viability exerted by EPA, the most immunosuppressive fatty acid. Similarly, measurement of the oxidative process by
NBT
reduction in cells treated with EPA was markedly increased. Nevertheless, the
proteasome
activity as a mechanism that participates in T-cell activation was not modified by direct action of the different fatty acids on the in vitro cultures. Overall, these results underline the differential role of several fatty acids (particularly long-chain n-3 polyunsaturated fatty acids) in order to modulate many functions of the immune system.
...
PMID:Modulatory effects of long-chain n-3 fatty acids on cell functions. 1211 28
Babesia microti is an emerging zoonotic pathogen that is transmitted by ticks and parasites and propagates in mammalian erythrocytes. Thioredoxin reductase (TrxR) plays a crucial role in B. microti survival by maintaining cellular redox homeostasis. In the present study, 4-nitro-2,1,3-benzothiadiazole (4-NBT) was selected as a specific B. microti TrxR inhibitor by comparing rat and parasite TrxR inhibition levels. Reactive oxygen species (ROS) levels were evaluated using flow cytometry, and in B. microti treated with 4-
NBT
, ROS levels increased with increasing inhibitor concentration. Furthermore, the inhibitor treatment increased lipid peroxidation and protein carbonyl levels, thus indicating a state of oxidative stress. While B. microti treated with 4-
NBT
appeared to lose the ability to multiply in mice, the fastigium of parasitemia between the treated and control groups was comparable. Furthermore, a TUNEL assay showed that 4-
NBT
induces apoptosis in B. microti. Proteomic analysis of B. microti treated with 4-
NBT
detected 960 proteins. Label-free quantitative proteomic analysis identified 118 proteins that were significantly up-regulated and 37 that were significantly down-regulated in the treatment group relative to the control. Of the differential proteins,
proteasome
and ribosomal subunit expression was up-regulated, thus suggesting that redundant proteins may be damaged by oxidation and waiting for degradation, while proteins for subsistence are waiting for de novo synthesis. Moreover, the findings obtained herein suggest that the DNA and lipids were also damaged and awaiting synthesis or repair. In conclusion, TrxR dysfunction in B. microti results in the breakdown of redox homeostasis and promotes apoptosis.
...
PMID:4-NBT, a specific inhibitor of Babesia microti thioredoxin reductase, affects parasite biochemistry and proteomic properties. 3115 24