Tumorigenicity of nickel subsulfide in Strain A/J mice.

The pulmonary tumor response of Strain A mice has been reported to be a rapid and efficient predictor of carcinogenic potential for a variety of chemicals. The route of exposure has usually been by intraperitoneal injection (i.p.) of solubilized materials. We compared intratracheal (i.t.) instillation as a more representative route typical of human exposures, with i.p. injection of nickel subsulfide, a potent animal carcinogen. Animals were sacrificed either 20 weeks after the first dosing, or were held until 45 weeks after the first dosing. Urethane, a positive control, produced a significant increase in pulmonary tumor response after i.t. instillation as well as i.p. injection. For nickel subsulfide treated animals, there was no evidence of a dose-related increase in pulmonary tumor response in any i.p. or i.t. treatment group when compared with age-matched controls.

Pulmonary adenomas in A/J mice treated with silica.

This study was designed to test the pulmonary tumor response to intratracheally instilled silica in Strain A mice. Urethane was used as a positive control. Silica treatment was utilized to evaluate the effect of a potent fibrinogen on pulmonary adenoma formation in this unique animal model. Urethane produced an increase in pulmonary tumor response in this study in agreement with previous investigations. Also, the background incidence of adenomas was comparable to other studies. Silica treatment did not affect tumor incidence either in terms of percent of mice with adenomas or average number of adenomas per mouse.

Lifetime effects of intratracheally instilled nickel subsulfide on B6C3F1 mice.

A nickel subsulfide (Ni3S2) lung tumor model for the study of metal carcinogenesis was evaluated using intratracheally dosed B6C3F1 mice. A preliminary study of the survival of mice 14 days after a single intratracheal dose of Ni3S2 displayed an LD50 of 4 mg/kg. A lifetime study was then initiated using five graded doses of Ni3S2 or saline alone, administered once a week for 4 weeks. Animals which survived more than 60 days after the final dose were evaluated by histopathology. The study was terminated 27 months after initiation when approximately 50% of the control animals had died. There was no increase in neoplastic or nonneoplastic lesions observed in animals treated with Ni3S2 nor was there evidence of damage to the organs of the respiratory tract from this treatment. The lack of significant biological response appears to be the result of relatively low tolerated dose, efficient lung clearance, and repair of early lung lesions.

Yields and nutrient content of selected fresh fruits.

Proximate composition, edible yields, and selected nutrients were measured in cantaloupe, cherries, grapes, nectarines, plums, and watermelon sampled in six major U.S. markets. Yields were lowest (about 55%) for the melons, but were much higher (about 90% or above) for other fruits. Fruits were high in moisture, low in protein, fat, and energy. The estimated carbohydrate content ranged from about 8% for the melons to 17% for cherries. Vitamins A and C were present in moderate concentrations, but fruits were found to be low in vitamin B-6, folic acid, and pantothenic acid, as well as in the mineral elements.

Mineral analyses of vegetarian, health, and conventional foods: magnesium, zinc, copper, and manganese content.

The amounts of magnesium, zinc, copper, and manganese in 22 health and vegetarian foods and their conventional counterparts were measured. Increased levels of magnesium were associated with the presence of soy in vegetarian and health products. Zinc was low in the vegetarian meat and egg substitutes and in soy milk. Copper tended to be decreased in the vegetarian foods but increased in the health foods relative to levels in the conventional counterparts. Manganese levels were increased in most of the health and vegetarian food items relative to levels in the conventional foods.

Hepatic gluconeogenic enzymes, plasma insulin and glucagon response to magnesium deficiency and fasting.

Three experiments were conducted to assess the effects of magnesium deficiency on the activities of hepatic glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FDPase) and phosphoenolpyruvate carboxykinase (PEPCK). Experiment 1 was designed to determine if magnesium deficiency interfered with the gluconeogenic response to fasting. Rats were fed either a control (C) or magnesium-deficient (MD) diet for 12 days. One-half of each group of rats was fasted for 24 hours prior to death. Hepatic enzyme activities, plasma and liver magnesium, and whole blood glucose were measured. Activities of G6Pase and PEPCK were higher in fasted group C rats compared to fed group C rats. Activity of FDPase was lower. The response was similar in the MD groups. Comparison of C and MD groups indicated that magnesium deficiency was accompanied by an increase in PEPCK activity. To verify this result and to investigate the role of anorexia in producing increased PEPCK activity, experiment 2 included a pair-fed group (PF). The results indicated that anorexia was not responsible for increased PEPCK activity in MD rats. The relation of circulating insulin and glucagon concentrations to effects of magnesium deficiency was explored in experiment 3. A decreased insulin:glucagon ratio was observed in MD rats. The results of these experiments suggest that magnesium deficiency alters PEPCK activity by affecting secretion of pancreatic hormones.

Changes in potato tuber invertase and its endogenous inhibitor after slicing, including a study of assay methods.

The increase in the invertase activity of extracts from freshly cut potato (Solanum tuberosum L.) by "foaming," caused by selective denaturation of an endogenous invertase inhibitor, did not occur in extracts made from thin disks 2 days after slicing. Rather, foaming such extracts decreased invertase activity. Apparently, the inhibitor disappeared after slicing, and the enzyme became more labile to foaming. Such disappearance of inhibitor could account for up to 15% of the dramatic increase in total invertase activity that had occurred within 2 days after slicing. The difference between extracts from 0-day and 2-day slices was mainly in the first of two peaks of invertase activity eluted from diethylaminoethyl-cellulose columns. This peak was increased by foaming 0-day extracts, but even when foamed was much smaller than in 2-day extracts. The apparent loss in inhibitor was not caused by a decreasing susceptibility of the enzyme to the inhibitor. Both the increase in total invertase activity and the apparent loss of inhibitor after slicing were partially blocked by actinomycin D and completely blocked by cycloheximide.The presence of the inhibitor can lead to serious errors in the usual whole disk method of assay for invertase in slices. Ethyl acetate treatment reduces the solubility of the enzyme but does not inactivate the inhibitor.