Increase in life expectancy for mice fed diethylhydroxylamine (DEHA).

ICR Swiss strain mice were fed diethylhydroxylamine (DEHA) for life starting at 44 days of age at 10, 30, 100, and 300 mg/kg-day. The 10 and 30 mg/kg-day males and the 10 mg/kg-day females showed an increase in mean age of death of 76 (12.7%), 45 (7.5%), and 51 (7.4%) days, respectively, compared to controls. The respective confidence levels are 99.2, 90.0, and 92.9% that these results are significant by Student's t test.

The formation and inhibition of photochemical smog.

Photochemical smog is caused by a free-radical chain mechanism which converts NO to NO2. The NO2 further reacts to produce ozone, nitric acid, and peracylnitrates. This chain mechanism can be inhibited by suitable free-radical scavengers. The chemistry and toxicology of one such free-radical scavenger, diethylhydroxylamine, has been studied in depth. It has been shown to be effective, safe, and practical for use in urban atmospheres to prevent photochemical smog formation.

Effects of diethylhydroxylamine on hepatic microsomal lipid peroxidation and glutathione S-transferases.

The effects of diethylhydroxylamine (DEHA), a potent free-radical scavenger, on lipid peroxidation of rat liver microsomes were investigated in vitro. DEHA strongly inhibited ascorbate-dependent nonenzymatic microsomal lipid peroxidation. DEHA also completely inhibited nonenzymatic lipid peroxidation of heat-denatured microsomes, indicating that inhibition is protein-independent. DEHA only moderately inhibited NADPH-dependent enzymatic microsomal lipid peroxidation. DEHA has been shown to exhibit antitumorogenic properties. However, it had no significant effect on hepatic glutathione S-transferase, selenium-independent glutathione peroxidase, or selenium-dependent glutathione peroxidase activity in the DEHA-treated CD-1 (lCR) Br male mouse. This suggests that the mode of action of DEHA as an antitumorogenic agent may be different from that of butylated hydroxyanisole, whose antitumor function is attributed to induction of glutathione S-transferase activity.

The effect of diethylhydroxylamine on the incidence of tumors induced by benzo(a)pyrene in the mouse.

Groups of 20 male and 20 female CD-1(ICR)Br mice were treated either with 0, 3, 30, or 300 mg diethylhydroxylamine (DEHA)/kg-day (administered via the drinking water) from 57-112 days of age. For the four week period between 70 to 98 days of age, all animals received (via gavage) eight 1 mg doses of benzo(a)pyrene at 4 day intervals. One hundred thirty-seven animals survived the dosing period. Of these, 132 survived to 211 days of age at which time they were euthanized and necropsied. Gross lesions were observed only in the lungs and squamous portion of the stomach. Treatment with DEHA produced no significant effect on the lung tumor incidence of either sex. However, a significant increase in stomach tumors was observed in the females.

Teratology study in mice subjected to inhalation of diethylhydroxylamine, nitroethane, and diethylamine hydrogen sulfite.

Pregnant female mice were exposed from Days 6 to 17 of pregnancy to 8.9 +/- 2.0 ppm of diethylhydroxylamine and 14.3 +/- 2.0 ppm of nitroethane. Exposures were for 8.25 +/- 2.25 hours/day including weekends. The mice were also exposed continuously for 24 hours a day to the vapor of diethylamine hydrogen sulfite. The exposure produced no effect on the dams compared to the control group. There was no evidence of compound-induced terata, variation in sex ratio, embryotoxicity, or inhibition of fetal growth and development.