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Biomedical subjects

D L Avery

Publications and source records attributed to D L Avery.

11 recordsLinked to original sources
PubMed1980

Immunocompetence over the lifespan of mice exposed in utero to carbofuran or diazinon: I. Changes in serum immunoglobulin concentrations.

Pregnant F2 dihybrid mice received either a vehicle-control or 1 of 2 doses of the anticholinesterase pesticides Carbofuran (0.01 or 0.50 mg/kg) or Diazinon (0.18 or 9.00 mg/kg) in the diet daily throughout gestation. All mothers gave birth to viable, overtly normal offspring at term. However, a significant number (12%) of pups born to dams who received 9.00 mg/kg Diazinon died prior to weaning on day 28; necropsy findings were consistent with death from respiratory infection. There was no significant difference in mortality between control and pesticide-exposed offspring once they reached 28 days of age. Determinations of 5 different classes of serum immunoglobulin (Ig) concentrations (IgG1,IgG2a,IgG2b, IgA, IgM) at 101, 400 and 800 days of age indicated transient but consistent disturbances of 2 Ig classes in offspring as a result of prenatal pesticide exposure. IgG1 concentrations of male offspring exposed to 0.50 mg/kg Carbofuran or 0.18 mg/kg Diazinon were significantly elevated at 101 days but not at 400 or 800 days of age. IgG1 concentrations of female offspring exposed to 0.01 mg/kg Carbofuran or 9.00 mg/kg Diazinon were significantly depressed at 101 days but not different from controls at 400 or 800 days of age. Changes in IgG2b levels generally were similar to those recorded for IgG1 but of smaller magnitude. There were no significant effects on serum IgG2b or IgM concentrations, and only equivocal effects on IgA, as a consequence of prenatal exposure to either pesticide.

Animals↗
PubMed1977

Neurobehavioral effects of prenatal exposure to the organophosphate Diazinon in mice.

Pregnant mice were given to daily dose of 0, 0.18, or 9.0 mg Diazinon per kilogram body weight throughout gestation. Mothers of all dose groups gave birth to viable, overtly normal offspring. However, pups born to mothers receiving the higher dose of the organophosphate grew significantly slower than controls and remained significantly smaller at 1 month of age. Offspring of mothers receiving the lower dose apparently were unaffected, but systematic behavioral testing revealed subtle deviations from normal developmental ontogeny as shown by significant delays in the appearance of the contact placing reflex and of sexual maturity (descent of testes or vaginal opening). Mature offspring of mothers exposed to either dose of the pesticle displayed impaired endurance and coordination on rod cling and inclined plane tests of neuromuscular function. Offspring from the 9.0 mg/kg group, in addition, had slower running speeds in a Lashley III maze and less endurance in a swimming test. Brains obtained after sacrifice at 101 days of age revealed neuropathology in the forebrains of offspring born of mothers exposed to the higher dose. Despite functional impairments in offspring from the lower dose group, no corresponding brain pathology was observed by examination under the light microscope.

Animals↗
PubMedDate not supplied

Postnatal endocrine dysfunction induced by prenatal methylmercury or cadmium exposure in mice.

The subtle and delayed effects of two heavy metals, cadmium and mercury, on the pituitary-adrenal axis of mice were examined. Exeprimental animals were exposed to the toxins both in utero and neonatally via treated mothers' milk. Plasma levels of corticosterone, adrenal production of corticosterone in vitro, and the capacity of the liver to metabolize corticosterone in vitro were studied in these animals as adults. Exposure to methylmercury resulted in diminished hepatic metabolism of corticosterone in vitro due to a loss of liver mass. Adrenal function and plasma levels of corticosterone were unaffected by treatment. Cadmium-exposed animals examined at 277 days of age showed no significant differences when compared to untreated controls. However, when studied at 460-480 days of age, a sex difference in the response to cadmium exposure was noted. In males, the major effect was enhancement of hepatic reductive capacity, while in females, adrenal secretory capacity was enhanced. Possible mechanisms of action and consequences of these effects are discussed.

Adrenal Glands↗
PubMedDate not supplied

Postnatal endocrine dysfunction resulting from prenatal exposure to carbofuran, diazinon or chlordane.

Prenatal exposure to pesticides of three different classes initiated persistent postnatal endocrine dysfunction. Adrenal function and hepatic metabolism of corticosterone were studied in adult hybrid mice exposed during development to either an organophosphate (Diazinon), a carbamate (Carbofuran), or an organochlorine (Chlordane). Animals were exposed to relatively low levels of the toxins in utero and neonatally via the mothers' milk. Exposure to lower doses of the anticholinesterase compounds, Diazinon or Carbofuran, resulted in impairment of hepatic metabolism of corticosterone in vitro due to a loss in reductive capacity per unit liver weight. Plasma levels of corticosterone were also elevated in these animals, but without a concomitant increase in adrenal steroidogenesis in vitro. The effects of exposure to Chlordane were more complex. In male animals, exposure to lower doses of chlordane resulted in an increase in plasma corticosterone levels without an apparent increase in hepatic metabolism of corticosterone or adrenal steroidogenesis. In contrast, side-chain metabolism of corticosterone was decreased in female mice exposed to Chlordane. Similar effects on pituitary-adrenal function were not evident for the offspring of mice exposed to higher doses of the toxins. Possible mechanisms for this non-linear dose-response are discussed.

Adrenal Glands↗