Transient block of respiratory chain by @entity3789 triggers @entity1110 -diaphorase activity (a marker for XXXX synthase) in Dunning @entity35 prostatic epithelium.

@entity1 @entity263 @entity5 @entity1110 @entity8773 @entity281 @entity519 @entity3789 @entity842 @entity1576 @entity619 @entity35 @entity1604
Synthesis of @entity842 (NO) has been shown in the glandular epithelium of @entity1 prostate, with highest levels in the peripheral zone. This location is believed to be the main source of @entity263 . The ability of stromal cells to produce NO may contribute to the malignant process. Since solid @entity5 are prone to @entity519 and malignant progression, experiments were undertaken to test the effect of @entity1576 on the induction of @entity842 synthase (NOS) by a Dunning @entity35 prostatic epithelial line. A metastatic phenotype (Mat-LyLu) was treated in vitro with brief exposure to @entity3789 in order to mimic transient @entity519 stress. @entity1110 -diaphorase activities in @entity1604 -fixed cells was used to follow the expression of NOS. @entity1110 -diaphorase activity was found to be inducible by a range of factors, including mechanical damage and @entity281 . @entity3789 induced a dose-dependent staining that was statistically greater than in untreated cells. Consistent with diaphorase staining being a marker for the inducible isoform of NOS (iNOS), induction and enhancement of staining, respectively, was observed in response to treatment with lipopolysaccharide or withdrawal of @entity619 supplement. Results demonstrate that prostatic epithelia can be triggered in culture to express iNOS by transient oxidative stress in the form of respiratory poisoning by @entity8773 . Paradoxically, @entity842 production by epithelia within @entity519 zones of solid @entity5 may contribute to the promotion and/or inhibition of tumorigenesis.
