Children's frequency of consumption of foods high in fat and sodium

We administered a food frequency instrument to third-fifth grade students (n = 943) in four Texas schools. Comparison of foods reported on the food frequency questionnaire and on 24-hour dietary recalls (n = 7) produced a percent agreement of 83.3. The most frequent 25 foods accounted for 64.0% of food choices across all meals, 93.5% of breakfast choices, 76.4% of lunch choices, 70.5% of supper choices, and 76.0% of snack choices. Breads, milk, hamburger or steak, soda pop, tomato sauce or tomatoes, and cheese were the most frequently consumed foods. Fruits and juices accounted for 6.1% of total selections for boys and 6.6% for girls, while vegetables accounted for 15.7% of total selections for boys and 16.2% for girls. Fruit was more likely to be consumed for snacks than for meals, and vegetables were consumed in about the same frequency at lunch and supper and for snacks. We analyzed the total fat, saturated fat, and sodium content of the most frequently consumed foods. Seventeen of the top 25 foods for the total day and 13-16 for each meal or snack exceeded by at least 50% the recommended levels for fat, saturated fat, or sodium. The pattern of consumption was one of frequent consumption of a relatively small number of foods, many of which are high in fat or sodium.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane- induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.