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M H Lu

Publications and source records attributed to M H Lu.

42 records · Page 3Linked to original sources

In vitro estradiol synthesis and secretion by tadpole ovaries of different developmental stages.

The tadpole ovaries at TK stage XIX can synthesize and secrete estradiol (E2), yet it is unknown when this ovarian function starts and how it develops. To this end, the present work has been carried out. The ovaries of different developmental stages of tadpoles and young frogs of Rana catesbeiana were taken, cut into small pieces, and incubated for 6 hr at 20 degrees in Krebs-Ringer bicarbonate buffer. The media were then analyzed for E2 by radioimmunoassay. The results indicate that the tadpoles synthesize and release E2 as early as stage X, that E2 increases slowly and gradually through stage XXV, and that E2 increases rapidly in juvenile frogs. This trend of growth of the ovarian function in estradiol secretion in vitro is in accordance with that reported for female chick embryos. There exists the possibility that the growth of E2 secretion could be biphasic, one with slow increment of autonomous E2 secretion at early stages and the other with quick increase due to pituitary stimulation at the stage of metamorphic climax.

Analysis of Variance↗

Teratogenicity of ethylenethiourea and thyroid function in the rat.

Ethylenethiourea (ETU) was given by gavage at a dose of 40 mg/kg/day from Days 7 through 15 of gestation to hypothyroid and euthyroid rats, and to rats given exogenous thyroxine, to determine whether ETU teratogenicity occurs through alteration of maternal thyroid function. At sacrifice on Day 20 of gestation 84-100% of the fetuses in all groups given ETU were malformed regardless of the thyroid status of the dams. Ten percent of the fetuses of dams thyroparathyroidectomized at 75 days of age that were not given ETU were malformed; no malformations were noted among the fetuses of the other groups not given ETU. Hence, ETU was found to induce teratogenicity in rats but not through alteration of maternal thyroid status. In addition, it was determined that ETU lowered serum thyroxine concentration, that hypothyroidism itself increased the background level of malformations in the rat, and that hypothyroidism qualitatively and quantitatively increased the incidence of specific malformations after ETU administration.

Animals↗

Thyroxine-induced hyperthyroidism upon the reproductive performance of female rats.

L-Thyroxine (L-T4) was injected into mature rats daily at levels of 0, 3, 6, 12, 24, 48 and 96 mug/100 g body weight through estrous cycling, conception, pregnancy, parturition and 20 days of lactation. Mothers which lactated to 20 days were killed and mammary glands measured for DNA and RNA content. Those which were not able to maintain their pups were killed on the day when all pups died. Estrous cycling and pregnancy were not markedly effected by exogenous L-T4 at levels 3-96 times the normal thyroxine secretion rate in rats. After parturition the mothers on L-T4 above 12 mug did not allow the pups to suckle. As a result the pups died within 2-7 days after birth. Levels of L-T4 from 3 to 12 mug allowed lactation to progress, but survival of pups to day 20 of lactation was significantly lower than in the normal control group. The results of this study indicate that high levels of L-T4 inhibit mammary growth and mild secretion. This, in turn, results in the loss of pups, probably through depletion of prolactin as a result of higher metabolic rate due to hyperthyroidism.

Animals↗