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Biomedical subjects

J W Laskey

Publications and source records attributed to J W Laskey.

At least 37 records · Page 2Linked to original sources
PubMed1985

Effects of chronic high-level manganese exposure on male behavior in the Japanese quail (Coturnix coturnix japonica).

Male Japanese quail were chronically exposed to 5000 ppm manganese (Mn) as particulate manganese oxide (Mn3O4) in their diet from hatching to 75 days of age. No decrements in growth or in other indices of general toxicity were noted. There were significant (P less than .05) age-related increases in general locomotor activity in the control group, although no significant (.05 less than P less than .10) increases were seen in the Mn-treated group. Both control and Mn-treated groups had significant (P less than .05) age-related increases in aggressive behavior with an overall significant (P less than .05) treatment-related depression. Serum testosterone concentration was only slightly depressed (.05 less than P less than .01) in the 75 day-old, Mn-treated quail. Both the control and Mn-treated quail had higher liver Mn concentrations than previously reported in rodents. Both control and Mn-exposed quail accumulated 5 to 10 times more Mn in their livers than similarly treated rodents. This study indicated that the Japanese quail was less sensitive to particulate Mn3O4 exposure than rodents treated comparably.

Aggression↗
PubMed1984

Reproductive effects of low acute doses of cadmium chloride in adult male rats.

Adult male Sprague-Dawley rats were injected sc with cadmium (Cd, as cadmium chloride) in doses ranging from 1.6 to 152 mumol Cd/kg body weight (body wt). Fourteen days after dosing, animals were evaluated for reproductive damage. Evaluations for each animal included testes, seminal vesicles, and epididymides weights, vas deferens sperm concentration, and human chorionic gonadotropin (hCG)-stimulated serum testosterone concentration. Since 10 to 60% mortality occurred in the two highest dose groups (74 and 152 mumol/kg), no additional evaluations were conducted in these groups. The weights of the testes, seminal vesicles, and epididymides were reduced at least 40 to 50% in groups receiving 16 or 33 mumol Cd/kg while vas deferens sperm concentrations and hCG-stimulated serum testosterone concentrations were essentially zero. Significant depressions in the sperm concentrations and in the hCG-stimulated serum testosterone concentrations were found in animals receiving the two lowest doses (1.6 and 7.4 mumol Cd/kg) although no changes in tissue weights were observed in these animals. Curve-linear regression analyses for the dose responsiveness of these parameters demonstrated that serum testosterone concentration initially decreased at a rate of 19%/mumol Cd/kg, respectively, and was the most sensitive to Cd exposure. The initial rates of decrease for sperm concentrations and for seminal vesicles, testes, and epididymides weight were 6.45, 5.30, 4.19, and 2.45%/mumol Cd/kg, respectively, and were less responsive to Cd exposure than serum testosterone levels.

Animals↗
PubMed1984

Effect of benomyl on the reproductive development of male rats.

Benomyl, a systemic fungicide, was administered to male Sprague-Dawley rats during the prepuberal, pubertal, or postpubertal stage of reproductive development. Animals received 5 or 10 daily treatments of 0, 125, 200, 250, 500, or 1000 mg benomyl/kg . d by gavage. Observations were made at selected intervals after exposure and included hematological parameters, body weight, tissue weights, total epididymal sperm counts, vas deferens sperm concentration, serum follicle-stimulating hormone ( sFSH ) levels, and testicular histology. Data presented here suggest that there is an age-related difference in sensitivity to benomyl. Animals that received benomyl treatments during prepuberty showed no significant treatment effects in tissue weights, total epididymal sperm counts, vas deferens sperm concentration, or sFSH . Animals that received at least 250 mg/kg . d during puberty or postpuberty showed one or more of the following effects: decreased testicular or epididymal weights, decreased epididymal sperm count, decreased vas deferens sperm concentrations, and/or testicular lesions. Histological examination of testicular tissue indicated a higher incidence of diffuse hypospermatocytogenesis in pubertal (20% of the treated animals) and postpubertal (40% of the treated animals) animals that were exposed to benomyl. These values were compared with those of the treated prepubertal animals, which had a 10% incidence of diffuse hypospermatocytogenesis , and with all of the control animals, which had no occurrences of this testicular lesion.

Animals↗
PubMed1982

Effect of benomyl on reproduction in the male rat.

Adult Sprague-Dawley male rats (65 days of age) received 10 daily treatments of 0, 200 or 400 mg benomyl/kg/day by gavage. Body weight, tissue weights, total epididymal sperm counts and sperm concentration from the vas deferens were measured 14 days after the last treatment. Testicular histology was evaluated in the 0 and 400 mg/kg/day groups. Significant findings included 35-48% depressions in the total epididymal sperm counts and in the vas deferens sperm concentrations in adult animals treated with 200 or 400 mg/kg/day. Histological evaluations of testicular sections from 6 adult animals in the 400 mg/kg/day group indicated a slight to moderately severe hypospermatocytogenesis in 2 animals and a slight to severe generalized hypospermatogenesis in 2 animals. Caudal epididymis weight were significantly (P less than 0.05) depressed with benomyl treatment. No treatment effects were found in body weight, liver, kidney, tests, or seminal vesicle weights.

Animals↗
PubMed1982

Chronic ingestion of Mn3O4 by rats: tissue accumulation and distribution of manganese in two generations.

Sprague-Dawley rats were chronically exposed to particulate Mn3O4 through two generations. At specific ages, observations were made of growth, tissue content, and distribution of Mn and Fe as affected by chronic exposure to Mn through an Fe-sufficient diet and an Fe-deficient diet. Chronic dietary Mn3O4 resulted in dose-related increases in Mn accumulation, and a concomitant Fe deficiency promoted Mn accumulation. In general, the addition of substantial amounts of Mn to either diet depressed tissue Fe levels.

Aging↗
PubMed1982

Effects of chronic manganese (Mn3O4) exposure on selected reproductive parameters in rats.

Long-Evans rats were chronically exposed to dietary Mn3O4 beginning on d 1 of gestation and continuing through 224 d of age. Dietary concentrations of Mn, as Mn3O4, were 350, 1050, and 3500 ppm and were applied in either a normal Fe 240 ppm) or a low-Fe (20 ppm) basal diet. General toxic effects were apparent in young animals at a dietary dose of 3500 ppm Mn and were enhanced by concomitant Fe deficiency. Fertility was reduced in the group exposed to 3500 ppm Mn with a diet containing sufficient Fe. Male reproductive development was delayed by Mn treatment, as measured by testes weight, sperm count, and serum follicle-stimulating hormone and testosterone concentrations.

Animals↗
PubMed1981

Chronic ingestion of Mn3O4 by young rats: tissue accumulation, distribution, and depletion.

Mn accumulation, distribution, and disappearance were evaluated in selected tissues of preweanling rats dosed daily with particulate Mn3O4 for 12 or 27 d postpartum. Significant findings include a high rate of Mn absorption and localization in tissues, especially the cerebrum, hypothalamus, and pituitary. In these tissues, the return of Mn concentrations to control levels was much slower when Mn dosing was continued beyond 18-20 d postpartum.

Animals↗
PubMed1980

Chronic manganese oxide ingestion in rats: hematological effects.

Hematological values were studied in Long Evans rats after chronic exposure to manganese oxide (Mn3O4). Data were obtained at selected ages from the P0 through the F2 generation. Effects of exposure to Mn3O4 during Fe deficiency were determined by placing half of the animals on a low-Fe diet (20 mg/kg) while the other half were maintained on a normal-Fe diet (240 mg/kg). Animals treated with Mn3O4 and maintained on a normal-Fe diet showed little variation from controls through 100 d of age. However, animals (24-100 d of age) maintained on a low-Fe diet and receiving Mn treatment during the prenatal and postnatal periods developed microcytic anemia. Irrespective of the dietary Fe level, serum creatinine levels decreased in the groups receiving 400 and 1100 ppm Mn while serum Ca and P levels increased in the group receiving 1100 ppm Mn at 100 d of age. Serum values for lactate dehydrogenase, alkaline phosphatase (100 d of age), and serum glutamic-oxaloacetic transaminase (224 d of age) were elevated for all animals on low-Fe diets. Globulin, albumin (100 d of age), and glucose (224 d of age) levels were depressed in all low-Fe groups.

Animals↗
PubMed1980

Chronic manganese oxide administration to preweanling rats: manganese accumulation and distribution.

Mn accumulation was evaluated in selected tissues of preweanling rats dosed daily with particulate Mn3O4. Significant findings include a high rate of Mn accumulation in the preweanling rat; a Mn dose-related acceleration of postpartum liver iron depletion; a Mn dose-related depression in red blood cells, hematocrit, hemoglobin, body weight, and survival by 21 d postpartum; and a Mn distribution in tissues with liver greater than brain greater than or equal to kidney greater than testes at 18-21 d of age.

Aging↗
PubMed1980

Multivariate analysis of the effects of manganese on the reproductive physiology and behavior of the male house mouse.

Chronic exposure to Mn3O4 in the diet at 1050 ppm Mn retarded the sexual development and lowered reactive locomotor activity levels in male mice. A multivariate analysis of variance indicated that testis, seminal vesicle, and preputial gland weights were significantly smaller as a result of Mn administration. These results support earlier observations of altered locomotor activity levels and reproductive development in male rats in the absence of other signs of toxicity.

Animals↗
PubMed1975

Some aspects of brain neurochemistry after intrauterine exposure to tritium.

Rats were continuously exposed to tritiated water (0, 1, 10 and 100 muCi HTO/ml body water) from conception to birth. Calculated, cumulative whole-body doses to the embryo and foetus were approximately 0, 6-6, 66 and 660 rad. The levels of several enzymes and established or presumptive central nervous system neurotransmitters were examined postnatally in whole brains. These were norepinephrine (NE), dopamine (DA), acetylcholinesterase (AChE) and monoamine oxidase (MAO). Intrauterine exposures to doses as low as 66 rad produced measurable and persistent decreases in brain weight and increases in NE concentrations at 21 and 45 days postnatally. No differences from control values were seen in the rate of turnover of NE or the concentrations of DA, AChE or MAO at 45 days. Exposure in utero to 6-6 rad produced no detectable postnatal effects on the brain neurochemical parameters measured.

Acetylcholinesterase↗
PubMed1975

Neoplastic and life-span effects of chronic exposure to tritium. II. Rats exposed in utero.

A study was conducted to determine the effects on neoplasia incidence and life-span of exposure in utero to a major environmental radionuclide. Sprague-Dawley rats were continuously exposed to tritiated water (HTO) from conception through birth in doses of 0, 1, 10, 50, and 100 muCi HTO/ml body water. HTO administration was terminated at birth. Calculated cumulative doses during gestation were approximately 0, 6.6, 66, 330, and 660 rads of total body irradiation. Under these exposure conditions, the two highest doses resulted in sterile offspring. Animals surviving through 30 days postnatally were defined as the study population and observed until their deaths. Intrauterine exposures to doses up to 66 rads had no significant effects on either sex with respect to life-span, overall neoplasia incidence, incidence rate, or onset of mammary fibroadenomas. Females exposed to 330 or 660 rads were sterile and had lower incidence rates of mammary fibroadenomass than did controls; at 660 rads females had a lower incidence of overall neoplasia and reduced mean life-spans. Sterile male offspring had reduced mean longevity after irradiation at 660 rads. Regardless of dose group, females had significantly higher incidences of neoplasia and longer life-spans than males.

Adenofibroma↗
PubMed1975

Developmental and behavioral changes in the rat during chronic exposure to lead.

Young male and female Sprague-Dawley rats were given drinking water containing 5 or 50 ppm Pb for 40 days prior to mating. Pregnant females were continued on these regimens throughout gestation and lactation. After weaning the offspring were similarly exposed through adulthood. Reflex development, body weights, and locomotor activity were measured in the offspring. Significant delays were noted in the development of the righting reflex at 5 and 50 ppm and in eye opening at 50 ppm. No difference was observed in development of the startle reflex at either dose. Mean body weights of treatment groups during this developmental period were not significantly different from controls. Locomotor activity was measured in adult males utilizing a residential maze. Both levels of lead produced a significant reduction in locomotor activity. When groups were treated with d-amphetamine (4.0 mg/kg subcutaneous), lead treatment caused a dose-related diminution in the amphetamine-induced hyperactivity. These results indicate that rats exposed to low levels of lead from conception until adulthood show a delay in nervous system development. As adults, these animals exhibit hypoactivity and decreased responsiveness to amphetamine.

Aging↗
PubMed1975

Neoplastic and life-span effects of chronic exposure to tritium. I. Effects on adult rats exposed during pregnancy.

Female Sprague-Dawley rats were continuously exposed to equilibrium levels of tritiated water (HTO) during pregnancy. The tritium activities were 1, 10, 50, and 100 muCi HTO/ml body water which provided cumulative, whole-body radiation doses of approximately 6.6, 66, 330, and 660 rads. Administration of the radioisotope was terminated at parturition. Throughout their life-spans and at autopsy, the dams showed an increased incidence of mammary fibroadenomas at exposure to 330 and 660 rads. Although the data for the incidence of malignant mammary neoplasms were consistent with a linear dose response, the small numbers of tumors preclude specific definition of the dose-response curve. Postexposure life-spans for dams chronically exposed to 66, 330, and 660 rads during pregnancy were reduced by 14, 24, and 22%, respectively. Accelerated aging was also demonstrated in these rats: The mean age for mammary fibroadenoma onset decreased with an increasing dose of radiation.

Adenofibroma↗