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Biology of Reproduction, Vol 23, 445-451, Copyright © 1980 by Society for the Study of Reproduction
1 Laboratory of Human Reproduction and Reproductive Biology,
Department of Anatomy and Department of Physiology,
Harvard Medical School,
Boston, Massachusetts 02115 The effect of nicotine on oviducal lactate dehydrogenase (LDH) activity during early pregnancy
was investigated in the rat. Rats were injected s.c. with either nicotine (7.5 mg nicotine tartrate) in
0.2 ml saline or with saline (0.2 ml) twice daily from the morning of proestrus (Day 0 of pregnancy) until the day of sacrifice. Rats were sacrificed between 1000 h and 1200 h on Day 2 or Day
3 of pregnancy; the oviducts were removed, and oviducal flushings collected, and the oviducts
homogenized. The flushings and homogenates were analyzed electrophoretically and spectrophotometrically to determine the LDH isozymal distribution and the total specific activity of the
enzyme, respectively. Compared with the flushings of control rats, the flushings of nicotine-treated rats showed a
significant increase in specific activity of LDH in pregnant rats on both Day 2 and Day 3. Although
the specific activity of the enzyme in the Day 2 oviducal homogenates was unaffected by nicotine,
it was significantly increased in the Day 3 experimental samples. No LDH-4 isozyme was detected
in either the oviducal homogenates or the flushings of any of the groups of rats. There was no
alteration in the distribution of any of the isozymes or in the percentage of B subunits in the Day 2
oviducal homogenates of the nicotine-treated rats compared with the controls. In the Day 3
samples, the concentration of LDH-5 relative to the total was significantly less in the experimental
group, and the percentage of B subunits was significantly greater in this group. Nicotine caused
marked alterations in the relative concentrations of LDH isozymes in the oviducal flushings of both
groups of pregnant rats; the percentage of B subunits was significantly increased in the nicotinetreated Day 2 pregnant rats but was significantly decreased in the Day 3 experimental group. Nicotine was found to induce a 12 h delay in cleavage of rat ova from the 2-cell to the 4-cell
stage, confirming a previous finding. It is concluded that unless LDH exerts an inhibitory effect on
development at the high concentrations found in the oviduct of the nicotine-treated rats, an
additional mediator must be implicated in the regulatory function of nicotine on the development
of the rat ovum.
Note:
ACKNOWLEDGMENTS
This study was supported by a grant from the
Council for Tobacco Research, Inc., New York, NY.
The authors thank Mrs. S. Nieland for her help in the
preparation of the manuscript.
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