Antioxidant activity of fish sauces including puffer (Lagocephalus wheeleri) fish sauce measured by the oxygen radical absorbance capacity method.

Fish sauces are fermented seasonings traditionally used throughout Asia, including Japan. Here, we report on the antioxidant activity of 30 fish sauces, among them a puffer fish sauce developed specifically for this study. To determine the antioxidant activity (i.e., the peroxyl radical elimination capacity) of the fish sauces, the oxygen radical absorbance capacity (ORAC) was measured. ORAC values ranged between 104 µmol (flatfish sauce 1) and 103 µmol (sandfish sauce) trolox equivalent (TE)/100 ml of fish sauce. Hydroxyl radical scavenging activity (IC50) was measured using electron spin resonance. IC50 values ranged between 0.081% (puffer fish sauce) and 0.653% (sardine fish sauce 7). Puffer fish sauce had a high ORAC value (8,365 µmol TE/100 ml) and the highest hydroxyl radical scavenging activity (0.081). The relationship between the ORAC and IC50 values of the 30 fish sauces was determined to be intermediate (r =-0.521, p=0.01).

Lecithinized superoxide dismutase suppresses free radical substrates during the early phase of burn care in rats.

Severe hypovolemia is caused by an increase in blood vessel permeability in the early phase after an extensive burn; massive fluid volume replacement has been used for the treatment of this condition. The release of oxygen free radicals and chemical mediators, especially from skin tissue, induces the increase in blood vessel permeability. Free radical burst is associated with ischemia-related skin tissue injury. Although various antioxidant therapies have been used to inhibit the consequences of hypovolemia, an effective method has not been established. To elucidate the protective effects of lecithinized superoxide dismutase (PC-SOD) as an antioxidant agent. Each rat sustained a 30% total body surface area burn (n = 20) on the back by the Walker and Mason method were allocated into three groups: (1) no treatment group (n = 6), (2) a low dose of PC-SOD (0.67 mg/kg) group (n = 7), and (3) a high dose of PC-SOD (1.33 mg/kg) group (n = 7). The concentrations of malondialdehyde and SOD in the serum, skin tissue, and lung tissue were measured in each group 1 hour after burning. Both low and high doses of PC-SOD prevented malondialdehyde concentration associated with free radical burst after burning compared with the no treatment group (P < .05); serum (27.7 +/- 6.8, 10.8 +/- 2.7, and 12.1 +/- 2.8 nmol/L), skin tissue (2251.3 +/- 560.5, 802.7 +/- 228.8, and 790.1 +/- 188.3 nmol/wet.g), and lung (157.3 +/- 19.5, 109.1 +/- 23.9, and 81.9 +/- 20.3 nmol/wet.g). These data suggest that PC-SOD may be a protective agent against free radical-induced vasodilatation caused by severe, extensive burns.

The therapeutic efficacy of edaravone in extensively burned rats.

BACKGROUND: Extensive burn injury leads to production of free radicals subsequent to massive fluid resuscitation, which in turn increases the risk of acute lung injury. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a novel free radical scavenger, is clinically effective in improving the prognosis after cerebral infarction. However, the effect of edaravone against extensive burn injury has not been tested. Objected To evaluate whether edaravone can reduce free radical precursors in a 30% burn model in rats. DESIGN: Prospective, randomized controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats weighing 200 to 220 g. MAIN OUTCOME MEASURES: All rats (n = 10) were given a 30% full-thickness burn according to the Walker and Mason method. Immediately after the burn, edaravone was injected into the rats (n = 5) intraperitoneally at a dose of 9 mg/kg. One hour after burn injury, blood and tissue samples were collected to analyze free radical changes of serum and tissue malondialdehyde (MDA) and xanthine oxidase (XOD) and lung white blood cells. RESULTS: Statistical significance was found between nontreatment and edaravone treatment relative to serum MDA (mean +/- SD, 2.50 +/- 0.54 vs 1.74 +/- 0.29 nmol/mL), serum XOD (mean +/- SD, 5.04 +/- 1.67 vs 2.26 +/- 0.83 U/L), tissue MDA (mean +/- SD, 1268.7 +/- 289.9 vs 569.1 +/- 135.9 nmol/mg protein), tissue XOD (mean +/- SD, 256.3 +/- 58.1 vs 50.96 +/- 19.60 mU/g tissue), lung white blood cells (mean +/- SD, 3088 +/- 1144 vs 1542 +/- 575 mU/g tissue), and lung XOD (mean +/- SD, 428.3 +/- 210.5 vs 81.8 +/- 36.0 nmol/mg protein). CONCLUSIONS: Edaravone treatment induces significant reduction of free radical precursors and their metabolites compared with controls in burn rats. This suggests that edaravone could be helpful in the clinical treatment of large burns.