An interpretation of toxicity response of bobwhite quail with respect to duration of exposure.

Avian dietary toxicity tests were conducted with seven pesticides, two age groups (2 and 16 weeks old) of northern bobwhite (Colinus virginianus) and two durations (5 and 28 days) of exposure. Results were analyzed with an emphasis placed upon comparing mortalities on similar test conditions. An analysis that used the entire dose-time-response results led to the calculation of a common measure (asymptotic rate e) of temporal development of the response surface and served as a basis of comparison of diverse test results. The asymptotic median lethal concentrations were designated by ALC50 and the median lethal concentrations at the end of a test period by LC50. It was found that: (1) Young birds in 5- and 28-day tests were more sensitive to incremental increases in the duration of exposure than adults. (2) Young birds were less sensitive to incremental increases of dietary concentration than adults only in the 5-day test and displayed delayed response patterns in six of seven chemicals in those tests. (3) LC50 values of 5-day tests of young birds were greater than LC50 values of 28-day tests, but the corresponding ALC50s were smaller in 5-day tests than 28-day tests. (4) ALC50s for 28-day tests were lower for young birds than for adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Feeding supplemental iodine to adult mink; effect on thyroid hormones in adult and offspring.

We fed adult mink diets containing supplemental iodine, from 0 to 320 ppm, for one or seven months prior to breeding. Blood samples collected from the adults and their offspring (kits) at 4 wk post-partum were assayed for total thyroxine (T4), triiodothyronine (T3), reverse T3 (rT3), and T4-binding indices. As expected T4 concentrations of the adult and kit mink varied inversely with the level of supplemental iodine. In addition, T3 and rT3 concentrations decreased gradually in kits from the long-term experiment in response to the increased dietary iodine of the dams. T3 concentrations of kits from dams fed iodine short-term decreased markedly while rT3 concentrations were elevated greatly in response to increased dietary iodine of the dam. These decreases in hormone levels are due to serum iodine blocking the thyroid uptake of iodine and subsequent decrease of hormone synthesis. Excess iodine may also block the effect of thyroid stimulating hormone. The T4-binding indices of the adults, in general, were depressed, while the T4-binding indices of the kits were more variable. These effects are probably due to fluctuations in thyroglobulin.

Effect of an environmental contaminant, diisopropyl methylphosphonate, on the blood pressure of the mallard.

During a toxicological test using diisopropyl methylphosphonate (DIMP) on mallards, an anaesthesia-like response was noted after oral dosing. In order to further elucidate these effects, arterial blood pressures were determined both pre- and post-dosing on adult male and female mallards by cannulation of the left carotid artery. A significant decrease in systolic, diastolic, and mean blood pressure was noted after the oral administration of DIMP. There was no significant difference in response between males and females. During the first 30 min after dosing, systolic pressure fell from an average of 158 mmHg, to 94 mmHg, diastolic decreased from 127 mmHg to 63 mmHg, and mean blood pressure dropped from 138 mmHg to 75 mmHg. However, there was no significant effect on pulse pressure, heart rate, or respiratory rate. These results are compared to physiological data cited in the literature for various CNS-acting drugs on mallards.

Changes in ring-necked pheasants' (Phasianus colchicus) egg formation time, oviposition lag time, and egg sequence length due to ahemeral light-dark cycles.

A total of 108 pheasant hens was exposed to either a conventional 24-hr (14L:10D), an ahemeral 22-hr (14L:8D), or an ahemeral 26-hr (14L:12D) light-dark (L:D) cycle. Total lag time for each egg sequence was greater in the ahemeral cycles than in the conventional L:D cycle, resulting in significant (P less than .05) differences in egg formation times (EFT) or intraclutch intervals of 26.4, 25.8, and 27.5 hr, respectively. The EFT under the ahemeral 26-hr L:D cycle was synchronized (within 1.5 hr) with the length of the L:D cycle. This light cycle resulted in the longest egg sequences (average 8.5 eggs per sequence) produced under any of the three L:D cycle treatments due to a shorter pause in oviposition. Values were significantly (P less than .05) different from the average values obtained under the conventional 24 hr L:D cycle (4.9 egg per sequence) and ahemeral 22 hr L:D cycle (3.5 eggs per sequence).

Ahemeral light-dark cycles and egg production parameters of ring-necked pheasants (Phasianus colchicus).

The effects of two ahemeral light-dark (L:D) cycles on ring-necked pheasant egg production were investigated in this experiment. Three groups of 36 female and 12 male 10-month-old birds were exposed to control 24-hr (14L:10D), ahemeral 22-hr (14L:8D), or ahemeral 26-hr (14L:12D) L:D cycle. Average percent hen-day egg production (HDEP) was 63.8 for hens exposed to ahemeral 26-hr L:D cycle compared with 55.6% HDEP for the controls. Although this was not significant (P less than .05). It suggests a trend for pheasants exposed to ahemeral L:D cycles to improve egg production. Ahemeral L:D cycles did not significantly (P greater than .05) affect egg mass, shell-less eggs, cracked eggs, egg hatchability, and embryonic mortality. Shell quality, measured by specific gravity and shell thickness, was significantly (P less than or equal to .05) reduced for eggs obtained from hens exposed to ahemeral 22-hr L:D cycle. Fertility of eggs from hens kept under ahemeral 26-hr L:D cycle was significantly (P less than or equal to .05) improved compared with fertility of eggs from controls (89.3 vs. 78.4). Results of this research suggest that long ahemeral L:D cycles do play a role in the improvement of pheasant egg production and egg fertility.

Toxicological manifestations of 2,4,5,2',4',5'-, 2,3,6,2',3',6'-, and 3,4,5,3',4',5'-hexachlorobiphenyl and Aroclor 1254 in mink.

Adult female mink were fed diets that contained 2.5 ppm Aroclor 1254, 0.1 or 0.5 ppm 3,4,5,3',4',5'-hexachlorobiphenyl (345 HCB), 2.5 or 5.0 ppm 2,4,5,2',4',5'-hexachlorobiphenyl (245 HCB) or 2,3,6,2',3',6'-hexachlorobiphenyl (236 HCB), or a control diet from 1 mo prior to breeding through parturition. All mink fed 0.5 ppm 345 HCB died within 60 d, while those fed 0.1 ppm showed 50% mortality after 3 mo exposure. Only one stillborn kit was whelped in the Aroclor 1254 group. No adverse reproductive effects were observed in the animals fed 236 HCB or 245 HCB. Plasma progesterone concentrations were significantly depressed by Aroclor 1254 and significantly elevated by 0.1 ppm 345 HCB. 17 beta-Estradiol concentrations were not significantly altered by any of the dietary treatments. Hepatic microsomal cytochrome P-450 concentrations were significantly elevated by all treatments except 236 HCB, with the largest increases occurring in mink exposed to Aroclor 1254 and 345 HCB. Aminopyrine N-demethylase activity was elevated by 5.0 ppm 245 HCB. Aroclor 1254 caused significant elevations in both benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase activities. Benzo[a]pyrene hydroxylase activities were also significantly elevated in mink fed 245 HCB and 345 HCB. Aroclor 1254 caused a significant elevation in cerebellar and hypothalamic norepinephrine concentrations and a significant elevation in hypothalamic dopamine concentrations. Cerebral dopamine was elevated by 0.1 ppm 345 HCB, while midbrain dopamine levels were depressed. Norepinephrine concentrations were significantly elevated by 5.0 ppm 236 HCB in the midbrain and by 5.0 ppm 245 HCB in the medulla.

Thyroid hormone changes in the bobwhite (Colinus virginianus) after hatching.

Total concentrations of thyroxine (T4) and triiodothyronine (T3) in plasma, and their biological half-lives were measured in adult and immature bobwhite. Concentrations of T4 and T3 decreased approximately 75% from Days 1 to 10 after hatching. After Day 10, the concentration of T4 did not significantly change as a function of age; however, the concentration of T3 doubled from Day 21 (275 ng/dl) to Day 29 (550 ng/dl) after hatching and remained significantly elevated above adult level (300 ng/dl) through Day 64. Changes in total concentration of T3 in plasma were not related to shifts in hormone utilization, as evidenced by biological half-life.

Perinatal hexachlorobenzene toxicity in the mink.

Adult female standard dark mink were exposed to hexachlorobenzene (HCB) at concentrations of 0, 1, and 5 ppm in the feed and bred with males on the same treatments. Female offspring were allowed to mature to 16-17 weeks and killed. At 16-17 weeks of age, HCB had no effect on body weights or liver weights. Hepatic cytochrome P-450 and ethoxyresorufin-O-deethylase were significantly increased 2.0- and 1.5-fold, respectively, in the 5-ppm treatment group. Electron microscopy failed to reveal proliferation of the smooth endoplasmic reticulum. No hepatic damage was observed. No changes in in vitro renal function, measured as accumulation of para-aminohippurate and tetraethylammonium by renal cortical slices, were detected in any treatment group. Histological examination of renal slices did not reveal any alterations in morphology. Fat was the predominate site of HCB disposition; samples from the 5-ppm treatment group contained 626.10 +/- 12.01 ng HCB/g tissue. Whereas perinatal HCB administration has profound effects on the survival of offspring born to exposed mink, only induction of hepatic mixed-function oxidases was observed in the surviving kits without any observable frank hepatotoxicity.

Distribution and excretion of hexachlorobenzene in bobwhite (Colinus virginianus).

After a single dose of [14C]hexachlorobenzene (HCB) via gavage into the crop, the accumulation of [14C]HCB in female bobwhite (Colinus virginianus) tissues occurred to the greatest extent in adipose tissue followed by skin, liver, brain, heart and kidney, whole blood, and muscle. There was a general relation between increasing HCB concentration and increasing fat content of the tissue. Absorption of [14C]-HCB was rapid with peak radioactivity occurring at 4 h in all tissues except for fat and skin, where it continued to rise until 32 and 16 h after dosing, respectively. Elimination of HCB from tissue was biphasic with phase I representing the combination of HCB excretion and HCB redistribution from tissue into fat stores. Phase II represented solely HCB excretion, which appeared to be a first-order process. The half-life of [14C]HCB in tissues, feces, and eggs ranged from 9-13 d regardless of HCB concentration. Radioactive HCB accumulation in egg yolk was a significant mechanism for the removal of this chemical from bobwhite and accounted for 50% of the total HCB excreted.

Differential sensitivity to the delayed neurotoxin tri-o-tolyl phosphate in several avian species.

Adult white leghorn chickens, ring-necked pheasants, mallards, bobwhites, and Japanese quail were administered single oral doses of tri-o-tolyl phosphate (TOTP) at levels of 125, 250, 500, and 1000 mg/kg body weight. Corn oil served as the vehicle control. At 24 h after dosing, half the birds from each group were killed for determination of whole-brain neurotoxic esterase (NTE) activity. The remaining birds were maintained for 21 d. Daily observations for the development of clinical signs typical of delayed neurotoxicity were begun 7 d after dosing and continued for the subsequent 14 d. In both the Japanese quail and bobwhite, all doses of TOTP resulted in NTE inhibition in excess of 70%, yet no birds of either species developed ataxia or paralysis. However, in the mallard none of the doses of TOTP caused inhibition of NTE activity greater than 61% nor resulted in the development of clinical signs. In the pheasant, all doses of TOTP caused at least a 70% inhibition of whole-brain NTE activity, yet only birds receiving 500 and 1000 mg/kg developed clinical signs. In the chicken, all TOTP doses caused inhibition of NTE in excess of 80%, and all doses resulted in clinical signs typical of delayed neurotoxicity.

Temperature regulation in adult quail (Colinus virginianus) during acute thermal stress.

1. Evaporative heat loss, O2 consumption, CO2 production, and internal body temperature were measured in unanesthetized, unrestrained bobwhite (Colinus virginianus) at specific ambient temperatures (Ta). 2. No significant change in body temperature occurred at any Ta tested, but metabolic heat production (H) increased from 42.17 W/m2 at Ta 35 degrees C to 102.89 W/m2 at Ta 10 degrees C. 3. Evaporative heat loss (E) increased approximately two-fold from Ta 10-35 degrees C, with E/H increasing exponentially over the same temperature range. 4. No significant change in thermal insulation occurred from Ta 10-30 degrees C. 5. Combined convective and radiative heat transfer for the bobwhite was 2.96 W/m2 X C from Ta 10-35 degrees C.

Excretion and placental and mammary transfer of hexachlorobenzene in the European ferret (Mustela putorius furo).

Female European ferrets (Mustela putorius furo) absorbed 98.5% of a single dietary exposure of hexachlorobenzene (HCB). The HCB was found to readily cross the placenta and to be excreted in the milk of pregnant/lactating ferrets. After consuming HCB-treated feed, ferrets raising offspring excreted 50% of the initial dose by 32 d, while unbred ferrets achieved this same degree of HCB elimination in 41 d. The percentages of HCB excreted via the urine and feces were approximately 5 and 45%, respectively, in both groups at the 50% stage of elimination. Adipose tissue was the most significant long-term repository for HCB in the ferret. The other tissues analyzed for [14C]HCB showed a general relationship of increased radioactivity with increased fat content of the tissue. The ferrets with nursing kits were able to significantly reduce their body burden of HCB when compared to unbred females. The developing ferret kits were subjected to HCB insult both in utero and via dam's milk. The ratio of milk to placental exposure in the growing offspring was calculated to be 31:1. Thus, in addition to any toxic effects HCB may have on the adult reproducing population, the placental and mammary transfer of HCB constitutes a potential threat to the developing and growing animal.