Showing posts with label nitrosative stress. Show all posts
Showing posts with label nitrosative stress. Show all posts

Thursday, June 24, 2010

Oxidative and nitrosative stress contribute to lupus disease activity

University of Texas Medical Branch researchers have uncovered an association between free radical-mediated reactions and the severity and progression of system lupus erythematosus (SLE). Higher levels of oxidative and nitrosative stress markers were found in SLE patients with greater disease activity suggesting a causal relationship. Full findings of the study are available in the July issue of Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology.


Oxidative and nitrosative stress contribute to lupus disease activity:

Sunday, September 6, 2009

Oxidative and Nitrosative Stress is Not All Bad!

As many of you know, most of HEIRS Environmental Illness Research is focused on how the impairment of Nrf2 effects these conditions. Several factors can play an important role including SNPs in the Nrf2, nutritional factors including malnutrition and hyperglycemia which can be the result of toxic insult on beta cells, endoplasmic reticulum stress etc. and other factors help to boost or better regulate it such as sulfurophane in broccoli. A new article has been published that describes how HO-1 through Nrf2 is an important adaptive response mediator to nitrosative stress and this process is sometimes called "hormesis or preconditioning." Wipedia describes hormesis as "enerally-favorable biological responses to low exposures to toxins and other stressors." (Wipedia) You may recall we have discussed hormesis at length and I have even published a link to a drawing that was published in Mattson's papers. You can see that drawing here. In this article Suhr writes, "nitrosative stress caused by reactive nitrogen species such as nitric oxide and peroxynitrite overproduced during inflammation leads to cell death and has been implicated in the pathogenesis of many human ailments. However, relatively mild nitrosative stress may fortify cellular defense capacities, rendering cells tolerant or adaptive to ongoing and subsequent cytotoxic challenges, a phenomenon known as 'preconditioning' or 'hormesis'. One of the key components of cellular stress response is heme oxygenase-1 (HO-1), the rate limiting enzyme in the process of degrading potentially toxic free heme into biliverdin, free iron and carbon monoxide. HO-1 is upregulated by a wide array of stimuli and has antioxidant, anti-inflammatory and other cytoprotective functions." As this author tries to point out, not all oxidative stress is bad and in fact, is necessary to activate adaptive metabolic processes in cells.

HEIRS Blog: Nrf2, HO-1,
HEIRS Library: Tag: Nrf2, HO-1,

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Article Title: Role of nrf2-mediated heme oxygenase-1 upregulation in adaptive survival response to nitrosative stress.Surh, Y.-J. J., Kundu, J. K. K., Li, M.-H. H., Na, H.-K. K., and Cha, Y.-N. N. (2009). Archives of pharmacal research, 32(8):1163-1176. http://www.citeulike.org/user/HEIRS/article/5728055
Hormesis. Wipedia. Retrieved on September 6, 2009.

Mattson, M. P., Son, T. G., and Camandola, S. (2007). Viewpoint: mechanisms of action and therapeutic potential of neurohormetic phytochemicals. Dose-response : a publication of International Hormesis Society, 5(3):174-186. http://www.citeulike.org/user/HEIRS/article/3812627