An appraisal of routine methods for the determination of the anodal isoenzymes of lactate dehydrogenase.
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Biomedical subjects
Publications and source records attributed to W G Brydon.
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Following a 7-day control period, 5 male volunteers consumed, on each of 23 consecutive days, a weight of xanthan gum equal to 15 times the current acceptable daily intake (10 mg/kg b.w.) approved by the EEC and by the Joint FAO/WHO Expert Committee on Food Additives; thus, the lightest and heaviest of the volunteers consumed 10.4 g and 12.9 g respectively of xanthan daily. Measurements before and at the end of the test period showed that the ingestion of xanthan, as a pre-hydrated gel, acted as a bulking agent in terms of its effects on faecal wet and dry weight and intestinal transit time but had no significant effect on plasma biochemistry, haematological indices, urinalysis parameters, glucose tolerance and insulin tests, serum immunoglobulins, triglycerides, phospholipids and HDL cholesterol, breath hydrogen and breath methane concentrations. There was a moderate (10%) reduction in serum cholesterol and a significant increase in faecal bile acid concentrations. The data indicate that the ingestion of xanthan caused no adverse dietary nor physiological effects in any of the subjects. In particular, all of the enzymatic and other parameters that act as sensitive indicators of adverse toxicological effects remained unchanged.
Following a 7-day control period, five female and five male volunteers consumed a weight of gellan gum corresponding to 175 mg/kg body weight for 7 days, followed by 200 mg gellan gum per kg body weight for a further 16 days. Measurements before and at the end of the 23-day test period showed that the gellan gum acted as a faecal bulking agent for the male volunteers and for four of the females. Dietary transit time increased for 2 females and 2 males, and decreased for 3 females and 3 males. Faecal bile acid concentrations increased for 4 females and for 4 males; the average increases were from 0.69 to 0.83 mmol/24 h (females) and from 1.22 to 1.44 mmol/24 h (males). Gellan gum ingestion had no significant effect on (a) plasma biochemistry parameters; (b) haematological indices; (c) urinalysis parameters; (d) blood glucose and plasma insulin concentrations; (e) breath hydrogen concentrations. There were no significant changes in HDL cholesterol, triglyceride or phospholipid concentrations. Serum cholesterol concentrations decreased significantly (P less than 0.1) by 13% on average for females, and by 12%, on average, for males. The data indicate that the ingestion of gellan gum at a high level for 23 days caused no adverse dietary or physiological effects in any of the volunteers. In particular, the enzymatic and other indicators of adverse toxicological effects remained unchanged.
Following a 7-day control period, five male volunteers consumed, on each of 23 consecutive days, a weight of methylcellulose (MC) equal to ten times the acceptable daily intake (25 mg/kg b.w.) approved by the EEC and the Joint FAO/WHO Expert Committee on Food Additives (JECFA). The MC was well tolerated; no allergic responses were reported. Measurements before and at the end of the test period showed that the ingestion of MC, as a pre-hydrated gel, acted as a bulking agent in terms of increased faecal wet (p less than 0.05) and dry weight, with intestinal transit time increasing for three but decreasing for two of the volunteers. Small changes, well within the normal ranges, occurred in some haematological indices, serum lipids and a few plasma biochemistry parameters. There were no changes in urinalysis parameters or breath hydrogen concentrations. There were small (p less than 0.05) reductions in faecal volatile fatty acids and neutral sterols (mumol/g dry weight). The decreases in blood glucose and plasma insulin after 60 min were also within the normal clinical range. The data provide no indications of any adverse effects of methylcellulose resulting from its ingestion for 23 days at the level of 250 mg/kg b.w.
Following a 7-day control period, during which sampling was carried out on two occasions (days 1 and 8), 10 female and 10 male healthy volunteers consumed a weight of gellan gum corresponding to 175 mg/kg body weight for 7 days (days 8-14) followed by 200 mg gellan gum per kg body weight for a further 14 days (days 15-28). The total period of ingestion (21 days) was followed by a further 7-day control period (days 29-36). 'Control' samples for haematology and plasma clinical chemistry were therefore secured on days 1, 8 and 36, and 'test' samples were secured on days 15, 22 and 29. In addition, 24 h samples were monitored by urinalysis, and 24 h faecal samples were monitored for occult blood three times each week. The major objectives were to supplement the data for gellan gum obtained previously, particularly in respect of changes in eosinophil concentrations, and to re-examine the responses of two male volunteers who had given indications of eosinophilia in a previous study. There was no such response by them, or by any of the other 18 volunteers, on this occasion.
Following a 7-day control period, five male volunteers consumed a weight of propylene glycol alginate corresponding to 175 mg/kg body weight for 7 days, followed by 200 mg propylene glycol alginate per kg body weight for a further 16 days. Measurements before and at the end of the 23-day period of dietary supplementation showed that propylene glycol alginate had little effect on faecal parameters (pH, water content, daily wet and dry weights). The dietary transit time remained constant for three volunteers, increased for one, and decreased for one. The ingestion of propylene glycol alginate had no significant effect on (a) haematological indices, (b) plasma biochemistry parameters, (c) urinalysis parameters, (d) blood glucose and plasma insulin concentrations, (e) breath hydrogen concentrations. No allergic responses were reported by, nor observed in, any of the volunteers. The study therefore indicates that the ingestion of propylene glycol alginate at a high level for 23 days caused no adverse dietary or physiological effects; in particular, the enzymatic and other sensitive indicators of adverse toxicological effects remained unchanged.
Following a 7-day control period, five male volunteers consumed a weight of sodium alginate corresponding to 175 mg/kg body weight for 7 days, followed by 200 mg sodium alginate per kg body weight for a further 16 days. Measurements before and at the end of the 23-day period of dietary supplementation showed that sodium alginate acted as a faecal bulking agent for all volunteers, giving a significant (p less than 0.01) increase in daily wet weight, and also increases in the water content and daily dry weight, but no change in faecal pH. Although the dietary transit time remained constant for two volunteers, it decreased for two, and increased slightly for one, with little resulting change in the overall mean value. The ingestion of sodium alginate had no significant effect on (a) haematological indices, (b) plasma biochemistry parameters, (c) urinalysis parameters, (d) blood glucose and plasma insulin concentrations, (e) breath hydrogen concentrations. No allergic responses were reported by, nor observed in, any of the volunteers. The study therefore indicates that the ingestion of sodium alginate at a high level for 23 days caused no effects other than those normally associated with a polysaccharide bulking agent; in particular, the enzymatic and other sensitive indicators of adverse toxicological effects remained unchanged.