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Barbiturate potentiation was observed in Japanese quail fed dietary levels of 4, 21, and 24 ppm Hg as methyl mercuric chloride. Gross symptoms of mercury poisoning were not observed until after BP was observed. After the initial increase in BP time was observed in the birds receiving 4 and 12 ppm mercury, there followed a plateau in response until those birds receiving 24 ppm Hg began to show gross symptoms of toxicity and the BP time markedly rose again. Pronounced BP persisted 7 weeks after removal of mercury from the diet reflecting the long biological half-life of mercury as the methyl derivative. Selenium effectively prevented BP after 7 days exposure to toxic levels of methyl mercury chloride. Therefore, results suggest that early toxic effects of mercury can be observed readily by BP and that this environmental contaminant may influence drug activity or increase the sensitivity of the nervous system to sodium pentobarbital.

The endosteal reaction, the initial step in the formation of medullary bone, was investigated in femurs of estrogen-treated male Japanese quail. Morphologically, the endosteal cells were in an undifferentiated state until 30 h after estrogen treatment and showed characteristics resembling those of resting cells. Many preosteoblasts were seen on the endosteum at 33 h, whereas mitotic figures and fully differentiated osteoblasts were recognized at 36 h after estrogen. The mitotic figures were observed among the preosteoblasts on the endosteum. Autoradiographs showed that the number of endosteal cells labeled by [3H]thymidine injected 1 h before sacrifice was maximal 27 h after the estrogen administration and decreased markedly by 30 h. When a single injection of [3H]thymidine was given at 26 h after estrogen, the highest percent of labeled endosteal cells was observed 1 h later (27 h after estrogen). Labeled preosteoblasts and osteoblasts were observed at 7 h (33 h after estrogen) and 10 h (36 h after estrogen), respectively. Our results show that under the influence of estrogen, endosteal cells are induced to maximally synthesize DNA about 27 h after estrogen. These cells appear to modulate into preosteoblasts in about 6 h and then divide via mitosis to become osteoblasts within an additional 3 h. The development of medullary bone induced by estrogen occurs in a sequential and predictable manner, which makes it a useful system for studying basic problems on bone cell differentiation.

Methiocarb (4-methylthio-3, 5-xylyl N-methyl carbamate, Mesurol, Bay (3744), a bird repellent, was fed in concentrations of 100 to 1,000 ppm to common grackles (Quiscalus quiscula), mourning doves (Zenaida macroura), and breeding pairs of coturnix quail (Coturnix coturnix) to investigate the possibility of cumulative intoxication. Although aversion to treated diets was readily apparent in most of the tests, the 28- to 30-day median lethal concentration (LC50) was determined to be greater than 100 ppm for grackles, 630 ppm (95% confidence limits, 480-830 ppm) for doves, and greater than 1,000 ppm for coturnix quail. Methiocarb appeared to be noncumulative when measured by an index of chronicity: birds consumed several LD50 doses during a day's feeding, and when deaths occurred, they appeared to be due to acute intoxication. Egg production and live chick production were not affected in coturnix fed 100 ppm but were reduced at 316 and 1,000 ppm.

Five experiments were conducted involving both juvenile and adult Bobwhite quail (Colinus virginianus) to study the toxicity of lead acetate, lead shot, powdered lead and antimony. Performance of juvenile birds receiving up to 1,500 p.p.m. of lead as lead acetate was not significantly influenced during the six-week experimental period. Feeding 3,000 p.p.m. lead as lead acetate was not significantly influenced during the six-week experimental period. Feeding 3,000 p.p.m. lead as lead acetate was associated with a significant depression of body weight and an increase in mortality. Feeding growing quail up to 2,000 p.p.m. lead from either lead acetate or powdered lead, 3 or 6% antimony (as % of shot dosage or 5 lead shot per week caused no significant effects upon either body weight or mortality. No significant trends were noted in body weight, feed intake, semen quality or organ weight of adult quail that received up to 1,500 p.p.m. lead from lead acetate. Dosing adult Bobwhite quail cocks with 10 or more lead shot per week caused a significant increase in nortality, and more than 90% of those dosed with 30 shot per week died by the end of four weeks.

When male and female coturnix quail (Coturnix coturnix) were given a single subacute oral dose (5.62 mg/kg) of the avian frightening agent 4-aminopyridine (4AP) and paired with untreated mates, there was no effect on the reproductive performance of males; egg production of females was reduced the third week after treatment but recovered during the fourth week. Chronic exposure to 31.6, 100, and 316 ppm of 4AP in the diet of mated pairs did not affect reproductive performance during or after the 4- or 6-week period the chemical was fed, but no birds fed 1,000 ppm produced live chicks after treatment began and all died within 3 weeks. The 28-day LC50 of 4AP was determined to be 447 ppm for male coturnix and 562 ppm for females. F1 progeny from quail fed 31.6, 100, and 316 ppm 4AP and randomly mated at maturity showed no reproductive effects from their parents' exposure.

We found that mercury potentiated the toxicity and biochemical effects of parathion. Male Coturnix quail (Coturnix coturnix japonica) were fed a sublethal concentration of morsodren (4 ppm as methyl mercury) for 18 weeks. This resulted in an accumulation of 21.0 ppm of mercury in the liver and 8.4 ppm in the carcass. Birds fed clean feed and those fed morsodren-treated feed were orally dosed with 2, 4, 6, 8,and 10 mg/kg parathion, and their 48-h survival times compared. The computed LD50 was 5.86mg/kg in birds not fed morsodren and 4.24 in those fed the heavy metal. When challenged with a sublethal, oral dose of parathion (1.0 mg/kg), morsodren-fed birds exhibited significantly greater inhibition of plasma and brain cholinesterase activity than controls dosed with parathion. Brain cholinesterase activity was inhibited 41% in morsodren-fed birds and 26in clean-fed birds dosed with parathion, which suggested that the increase in parathion toxicity in the presence of morsodren was directly related to the inhibitation of brain cholinesterase.