Acute inhalation experiments were conducted to determine 24-h LC50 values for adult Sprague-Dawley rats of both sexes exposed to vapors of methyl mercaptan and other reduced-S compounds for 4 h periods. Using calculated gas concentrations, the following LC50 value for each gas and combination was determined: metyhl mercaptan, 675 ppm; dimethyl sulfide, 40,250 ppm; dimethyl disulfide, 805 ppm; hydrogen sulfide, 444 ppm; and an equimolar mixture of methyl mercaptan, dimethyl sulfide, and dimethyl disulfide, 550 ppm. The effects of body and tissue weights, gross metabolic performance, O2 consumption, systolic blood pressure, various blood parameters, and intestinal transit time associated with 3-mo exposures of young adult male rats to chemically verified concentrations of 2, 17, and 57 ppm methyl mercaptan vapor are summarized in this report. No mortality was experienced by any group. Histopathological findings were essentially nil except for microscopic suggestions of liver damage. The most readily apparent phenomenon was the decrease in body weight. Average values of terminal body weights for all exposed groups were lower than that for the sham control group. This difference was significant in the 57 ppm group and followed a statistically significant dose-related trend.

Pregnant CF1 mice and New Zealand White rabbits were given methamphetamine hydrochloride intravenously during days 9-15 and 12-30 of gestation, respectively. Offspring of mice given 5.0 mg/kg on days 9-15 of gestation had less than 2% anomalies. When 10.0 mg/kg were given on days 9-15, a 13.6% incidence of anomalies was observed. Offspring of rabbits receiving 1.5 mg/kg of methamphetamine on days 12-15, 15-20, and 12-30 of gestation showed an incidence of fetal anomalies of 12, 4, and 15.5% respectively. Offspring sired by treated males showed no significant weight change and had no increased anomaly rate.Dexamphetamine sulfate is teratogenic in A/ J mice (Nora et al., '65) and possibly

The secretory and motor responses of the Brunner's gland region of the duodenum to luminal acidification were examined in rabbits anesthetized with urethan. Isomotic solutions of sodium chloride (pH 7.2) were perfused continuously through adjacent in situ segments. The pH of the perfusate of the proximal segment was changed to 2.0 for 30 min. Perfusion pressure (motor response) and volume and hexosamine concentration (secretory response) of the effluent were recorded for 3 h. The motor and secretory responses to luminal acidification were examined after intravenous (atropine) or intraluminal (lidocaine) pretreatment. Responses to intravenous infusions of serotonin or secretin were determined, also. Both atropine and lidocaine eliminated the initial motor and secretory responses of the proximal segment. Lidocaine eliminated the delayed secretory response of the distal segment. Serotonin caused initial motor and secretory responses, but secretin caused a delayed secretory response only. These results suggest that duodenal acidification elicits a two-phase increase in Brunner's gland secretion, the first being motor-dependent and the second motor-independent. The initial motor response was mediated by a local reflex composed of cholinergic and perhaps tryptaminergic receptors. The delayed secretory response was mediated by local and nonlocal, possibly hormonal, factors. Increased duodenal motility may provide a vehicle for the rapid expulsion of mucus, and thereby serve an important role in the function of the Brunner's glands.

No abstract