Yukihiro Tamura

Efficacy of selenium in tuna and selenite in modifying methylmercury intoxication.

Abstract Efficacy of selenium naturally occurring in tuna was compared to that of selenium in selenite with respect to protection against the toxicity of methylmercury. Male weaning rats were fed diets for 70 days which contained 20 ppm methylmercury chloride (MMC) and graded concentrations of selenium originating from either tuna or sodium selenite. Regardless of its origin, selenium showed protective effect, generally corresponding to its added levels (0.5, 1.0, 1.5 ppm) in terms of survival rate, morbidity and growth rate. Efficacy of selenium in tuna, as compared to that of selenium in selenite, was roughly equivalent in growth rate but approximately half as effective in preventing neurological manifestations. Possible mechanisms were discussed as regards protection offered by selenium and the discrepancy of efficacy between tuna selenium and selenite selenium in preventing neurological signs. This study seems to warrant further investigations upon the protective activity of naturally occurring selenium against methylmercury toxicity, particularly in those fish known to contain high concentrations of both methylmercury and selenium.

Interaction of dietary methylmercury and selenium on accumulation and retention of these substances in rat organs.

Abstract Four groups of male Wistar rats were fed the following regimen for 40 days: (1) 20 ppm methylmercury chloride (MMC); (2) 20 ppm MMC + 3 ppm sodium selenite; (3) 3 ppm sodium selenite; (4) basal diet. The basal diet which contained 0.4 ppm “organic selenium” originating mainly from fish meal and wheat was resumed on day 41. Protective effect of selenite over toxicity of methylmercury was observed in terms of both growth rate and morbidity. Concentrations of total mercury, methylmercury and selenium were determined on Days 0, 20, 41, 47, 54, and 61 in the brain, liver, kidney, and blood. It was noted that methylmercury increased accumulation of selenium in all the organs analyzed while selenium retention varied according to the type of selenium and the organs. Modification by selenite, despite its protective effect, remained equivocal in regard to the organ accumulation of mercury and its retention therein.

Degradation of Aflatoxins by Food Additives

Degradation of four aflatoxins (AFB1, AFB2, AFG1 and AFG2) by food additives was investigated. Pure aflatoxins were degraded by treatment with solutions of acidic food additives (hydrochloric acid:HCl and sulfuric acid:H2SO4), alkaline food additives (sodium bicarbonate:NaHCO3, sodium carbonate:Na2CO3, sodium hydroxide:NaOH, sodium sulfite:Na2SO3, and sodium hypochlorite:NaOCl) and neutral food additives (potassium metabisulfite:K2S2O5, sodium bisulfite:NaHSO3, sodium hydrosulfite:Na2S2O4, hydrogen peroxide:H2O2, sodium chlorite:NaClO2, and ammonium peroxodisulfate:(ÑH4)2S2O8). The aflatoxins were treated with these neutral food additives under several conditions, and the effects of treatment temperature, time, and concentration of food additives on aflatoxin degradation were studied. Potassium bromate (KBrO3), potassium nitrate (KNO3), and sodium nitrite (NaNO2) had no effect on aflatoxins. Of the aflatoxin added to corn, 20% AFB, remained after treatment with the solution of NaHSO3 (0.5%, 48 h), but all of the AFB1 was completely degraded by NaClO2 (0.25%, pH 4, 48 h) and (NH4)2S2O8 (0.25%, 48 h) at 60°C. Of the aflatoxins added to butter beans, less than 20 and 5% of AFB1 remained after boiling treatment with a 2 and 0.5% solution of Na2S2O4, respectively. These findings suggested that aflatoxins can be degraded or removed by treatment with food additives during food processing.

Tail rotation, an early neurological sign of methylmercury poisoning in the rat.

Abstract All of 95 Wistar rats on a diet containing 20 ppm of methylmercury and 0.1 ppm of selenium displayed “tail rotation,” namely, sustained vigorous circling movement of the tail when held up by the trunk, for 2 to 3 weeks prior to the onset of weight loss and of crossing and/or ataxia of the hind legs. With the onset of tail rotation morphological changes in the nervous system involved only the peripheral sensory nerves and their terminal corpuscles; mercury levels in the brain were two-thirds as high as those associated with crossing and ataxia of the hind legs. Ablation of visual and inner ear function did not seem to affect its directionality or velocity. This sign appears to be an earlier manifestation of peripheral sensory neuropathy induced by methylmercury.

Chronological relationship between neurological signs and electrophysiological changes in rats with methylmercury poisoning — special reference to selenium protection

In order to see chronological relationship between electrophysiological changes and “early” neurological sign (tail rotation) elicited in rats poisoned with methylmercury, we made serial measurements of amplitude of compound action potential and sensory nerve conduction velocity of the tail nerve in rats with five dose schedules [methylmercury vs selenium, (1)20 ppm : 0.1 ppm, (2)20 ∶ 0.3, (3)20 ∶ 0.6, (4)10 ∶ 0.1, (5)10 ∶ 0.6].We observed the following sequence in the onset of neuro-electrophysiolo-somatic signs: fall in compound action potential > decrease in sensory nerve conduction velocity > tail rotation > weight loss. Protective potency of dietary selenium against neurotoxicity of methylmercury was observed with regard to both electrophysiological changes and neurological signs.