BACKGROUND: Oxidative stress is related to various diseases, such as diabetes, cancer, inflammatory disease, and arteriosclerosis. The aim of this study is to evaluate enhancement effect in serum antioxidant capacity obtained from an antioxidative nutrient-rich enteral diet (AO diet). We also investigated the ability of the AO diet to attenuate lethality, the production of oxidized products, the production of inflammatory cytokines, and liver injury using lipopolysaccharide (LPS)-injected mice. LPS mice were used as a model to represent critically ill patients that have experienced a septicemia. METHODS: The AO diet contained polyphenol and enhanced vitamin C, vitamin E, and trace elements. Total antioxidant activities of the control enteral diet (Control diet) and the AO diet were measured by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azinobis-(3-ethylbenzthiazoline sulphonic acid; ABTS) radical-scavenging activities. Male BALB/c mice were fed either of these diets for 7 days and were injected with 5 mg/kg LPS. The survival of mice was monitored from day 0 to day 8. To evaluate oxidative stress, inflammation, and liver injury, blood and liver samples were collected, and tumor necrosis factor-alpha (TNF-alpha), interleukin-6, thiobarbituric acid-reactive substances (TBARS), protein carbonyl contents, aspartate aminotransferase, alanine aminotransferase, and radical-scavenging activities were measured. RESULTS: The survival rate of mice receiving the AO diet or the Control diet was 73.9% and 33.3%. In the AO diet group, levels of serum TNF-alpha, serum protein carbonyl contents, plasma, and liver TBARS were significantly lower than in the Control diet group. DPPH and ABTS radical-scavenging activities of the AO diet itself were significantly higher than that of the Control diet, and serum activities in the AO diet group were also higher. CONCLUSIONS: The antioxidative nutrient supplementation of an enteral diet may be useful and offer relief from septic symptoms.
BACKGROUND: Oxidative stress is related to various diseases, such as diabetes, cancer, inflammatory disease, and arteriosclerosis. The aim of this study is to evaluate enhancement effect in serum antioxidant capacity obtained from an antioxidative nutrient-rich enteral diet (AO diet). We also investigated the ability of the AO diet to attenuate lethality, the production of oxidized products, the production of inflammatory cytokines, and liver injury using lipopolysaccharide (LPS)-injected mice. LPSmice were used as a model to represent critically illpatients that have experienced a septicemia. METHODS: The AO diet contained polyphenol and enhanced vitamin C, vitamin E, and trace elements. Total antioxidant activities of the control enteral diet (Control diet) and the AO diet were measured by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azinobis-(3-ethylbenzthiazoline sulphonic acid; ABTS) radical-scavenging activities. Male BALB/c mice were fed either of these diets for 7 days and were injected with 5 mg/kg LPS. The survival of mice was monitored from day 0 to day 8. To evaluate oxidative stress, inflammation, and liver injury, blood and liver samples were collected, and tumor necrosis factor-alpha (TNF-alpha), interleukin-6, thiobarbituric acid-reactive substances (TBARS), protein carbonyl contents, aspartate aminotransferase, alanine aminotransferase, and radical-scavenging activities were measured. RESULTS: The survival rate of mice receiving the AO diet or the Control diet was 73.9% and 33.3%. In the AO diet group, levels of serum TNF-alpha, serum protein carbonyl contents, plasma, and liver TBARS were significantly lower than in the Control diet group. DPPH and ABTS radical-scavenging activities of the AO diet itself were significantly higher than that of the Control diet, and serum activities in the AO diet group were also higher. CONCLUSIONS: The antioxidative nutrient supplementation of an enteral diet may be useful and offer relief from septic symptoms.