Glutathione is Powerful Anti-Inflammatory

Date:   2/7/2009 10:18:16 PM ( 15 y ago)

cytokines are inflammatory agents in the body that create systemic inflammation and are associated with many diseases including heart disease, diabetes, cancer, graves disease, and many others.

the first study shows that boosting glutathione levels inhibited cytokine production. thats a good thing!

the second study's main goal was to study how consumption of glucose (sugar) stimulated cytokine production. they discovered that the more sugar you ate, the more cytokines you produced, and the more susceptible you would be to diabetes. however! something amazing happened when they administered glutatione before ingestion of the sugar...

"On another occasion, 10 control and 8 subjects received the same glucose pulses as above during an infusion of glutathione; plasma cytokine levels did not show any significant change from baseline after the 3 glucose pulses"

in other word even after three doses of glucose the patients' cytokine levels did not rise at all if they were given glutathione previously.

http://pen.sagepub.com/cgi/content/abstract/23/1/1


Treatment With Glutathione Precursor Decreases Cytokine Activity

Luis R. Pena, MD, Daniell B. Hill, MD, Craig J. McClain, MD


Background: Inflammatory cytokine activity is increased in many forms of experimental and clinical liver injury including alcoholic liver disease (ALD). Monocytes and Kupffer cells produce cytokines such as tumor necrosis factor (TNF), interleukin (IL)-8, and IL-6 in response to stimuli such as endotoxin (lipopolysaccharide [LPS]).

This cytokine production is regulated by the oxidative stress-sensitive transcription factor NF{kappa}B. Glutathione (GSH) prodrugs such as oxathizolidine-4-carboxylic acid (OTZ) can inhibit activation of NF{kappa}B and subsequent cytokine production in monocytes and Kupffer cells in vitro. The objective of this study was to treat stable cirrhotic patients with OTZ in vivo to evaluate its effects on monocyte cytokine production (TNF, IL-8, and IL-6) and whole blood GSH levels. Methods: Nine patients with stable cirrhosis received OTZ (70 mg/kg IV every 8 hours) for 9 days. Peripheral blood monocytes were obtained on study days 1 and 9, using density gradient centrifugation and adherence to plastic, and were stimulated with LPS (5 µg/mL) . TNF, IL-8, and IL-6 were measured in culture supernatants by enzyme-linked serum immunosorbent assay. Whole blood GSH levels were measured by high-performance liquid chromatography. Results: There was a significant decrease in monocyte TNF, IL-8, and IL-6 production after OTZ therapy. Patients with cirrhosis had significantly lower admission whole blood GSH levels compared with controls and GSH normalized with OTZ administration.

Conclusions: Treatment with the GSH prodrug OTZ inhibited monocyte cytokine production and increased whole blood GSH. This may have important therapeutic implications for multiple cytokine-mediated disease processes. ( Journal of Parenteral and Enteral Nutrition 23:1-6, 1999)

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http://www.mdconsult.com/das/citation/body/119414104-2/jorg=journal&source=MI...


Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. - Esposito K - Circulation - 15-OCT-2002; 106(16): 2067-72 (MEDLINE is the source for the citation and abstract of this record )

Abstract:

BACKGROUND: Circulating levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) are elevated in diabetic patients. We assessed the role of glucose in the regulation of circulating levels of IL-6, TNF-alpha, and interleukin-18 (IL-18) in subjects with normal or impaired glucose tolerance (IGT), as well as the effect of the antioxidant glutathione. METHODS AND RESULTS: Plasma glucose levels were acutely raised in 20 control and 15 IGT subjects and maintained at 15 mmol/L for 5 hours while endogenous insulin secretion was blocked with octreotide.

In control subjects, plasma IL-6, TNF-alpha, and IL-18 levels rose (P<0.01) within 2 hours of the clamp and returned to basal values at 3 hours. In another study, the same subjects received 3 consecutive pulses of intravenous glucose (0.33 g/kg) separated by a 2-hour interval. Plasma cytokine levels obtained at 3, 4, and 5 hours were higher (P<0.05) than the corresponding values obtained during the clamp. The IGT subjects had fasting plasma IL-6 and TNF-alpha levels higher (P<0.05) than those of control subjects. The increase in plasma cytokine levels during the clamping lasted longer (4 hours versus 2 hours, P<0.01) in the IGT subjects than in the control subjects, and the cytokine peaks of IGT subjects after the first glucose pulse were higher (P<0.05) than those of control subjects.

On another occasion, 10 control and 8 IGT subjects received the same glucose pulses as above during an infusion of glutathione; plasma cytokine levels did not show any significant change from baseline after the 3 glucose pulses. CONCLUSIONS: Hyperglycemia acutely increases circulating cytokine concentrations by an oxidative mechanism, and this effect is more pronounced in subjects with IGT. This suggests a causal role for hyperglycemia in the immune activation of diabetes.

 

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