Publication Date

1984

Document Type

Dissertation/Thesis

First Advisor

Prahlad, K. V.

Degree Name

M.S. (Master of Science)

Department

Department of Biological Sciences

LCSH

Paraquat

Abstract

Paraquat (1,1'-dimethyl, 4,4'-dipyridilium dichloride) selectively accumulates in the lungs of mammals after ingestion or injection, resulting in edema, necrosis and fibrosis. Hormonal and physiological imbalance are also evident after administration. The goal of this investigation was to determine what, if any, effects paraquat might have on lung development in the fetal rat since paraquat might either selectively accumulate in the fetal lung and cause damage or affect hormones which regulate lung differentiation and maturation. Pregnant animals were injected with either 1 or 4 mg of paraquat per kg maternal weight (sublethal doses) for three consecutive days at various times: either early, at midterm, or late in gestation. Animals were sacrificed on day 19 of pregnancy and fetuses were weighed and examined for external abnormalities. Two fetuses per litter were cleared and stained with Alizarin Red and Alician Blue for examination of bone defects. Fetal and maternal lung samples were frozen for glycogen and protein determinations. Fetal and maternal lung samples were also fixed for light and transmission electron microscopy. Radioactive paraquat uptake by fetal, maternal, and adult (nonpregnant rat) tissues was examined separately after injections of [methyl-¹⁴C] paraquat chloride. No effect of paraquat on maternal or fetal mortality or morphology was noted. Significant differences in fetal weight between control and experimental fetuses were obtained at both concentrations of paraquat treatment. Light and electron microscopic examinations revealed damage to maternal lung tissue but not fetal lung tissue. Radioactive paraquat was not accumulated to any extent by the fetal lung or liver tissues examined, but was concentrated in a similar fashion by both nonpregnant and pregnant rat tissue. The potential of paraquat as a teratogen is low, probably because it does not cross the placenta. Protection from toxicity by increased corticosteroid levels during pregnancy might have occurred, resulting in less damage to the maternal system and no subsequent effects in the fetus.

Comments

Bibliography : pages 57-62.

Extent

vii, 62 pages

Language

eng

Publisher

Northern Illinois University

Rights Statement

In Copyright

Rights Statement 2

NIU theses are protected by copyright. They may be viewed from Huskie Commons for any purpose, but reproduction or distribution in any format is prohibited without the written permission of the authors.

Media Type

Text

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