Extracts
from “Trace Elements in Human and Animal Reproduction” (ARTICLE)
by
E J Underwood. Published by Academic Press, 1979
Manganese Deficiency and Functions
Manganese and Reproductive Function Defective ovulation, testicular
degeneration, and infant mortality were observed in the earliest
studies demonstrating the essentiality of manganese in the diet of
rats. In the female, three stages of manganese deficiency can be
recognised. In the least severe state the animals give birth to viable
young, some or all of which exhibit ataxia. In the second, more severe
state the young are born dead or die shortly after birth. In the
third, acute stage of deficiency estrous cycles are absent or irregular,
the animals will not mate, and sterility results. A delay in the
opening of the vaginal orifice may also occur. The severely manganese
deficient male rat and rabbit exhibit sterility and absence of libido,
associated with seminal tubular degeneration, lack of spermatozoa,
and accumulation of degenerating cells in the epididymis. In guinea
pigs omission of manganese from the maternal diet increases the proportion
of young born dead or delivered prematurely and reduces litter size.
The feeding of low manganese rations to cows and goats causes depressed
or delayed estrus and conception, as well as increased abortion and
stillbirths and lowered birth weights.
Zinc Deficiency and Functions
Zinc and Reproduction Spermatogenesis and the development of the primary
and secondary sex organs in the male, and all phases of the reproductive
process in the female from estrus to parturition and lactation, can
be adversely affected in zinc deficiency.
The effects of zinc deficiency in the female depend on the severity,
timing, and duration of the deficiency. When Hurley and Swenerton fed
a nearly zinc free diet to female rats from weaning to maturity the
animals made no growth and displayed severe disruption of the estrus
cycles.
Brain Development and Behaviour. Zinc deficiency during the critical
period for brain growth permanently affects brain function. When this
deficiency is imposed throughout the latter third of pregnancy, brain
size is decreased, there is a reduced total brain cell number, and
the cytoplasmic nuclear ratio is increased, implying an impairment
of cell division in the brain during the critical period of macroneuronal
proliferation. In adult life male rats so treated display impaired
shock avoidance, and female rats are significantly more aggressive
at a high level of shock than adult female rats whose dams were zinc
sufficient during pregnancy. When the zinc deficiency is imposed from
birth to 21 days of age, brain size is diminished, brain DNA, RNA,
and protein concentrations are reduced and impaired maze acquisition
ability is evident in such animals when adults.
Retarded brain maturation, as indicated by reduced total cerebellar
lipid concentration, is evident in zinc deficient suckling rats and
a markedly lower rate of protein synthesis in the brain of zinc deficient
weanling rats.
Vanadium Functions and Requirements
Reproduction Rats consuming diets of less than 10 ppm vanadium over
several generations exhibit a marked impairment of reproductive performance
and increased pup mortality. Fertility was reduced slightly in third
generation females and markedly in fourth generation females, with
no such effects on control vanadium-supplemented animals. Pregnancies
per mating period and pup survival at 21 days were both reduced in
the vanadium deficient animals in two different strains of rats.
Nickel Deficiency and Functions
Rats fed diets containing 2-15 ppm nickel throughout fetal, neonatal
and adult live exhibited impaired growth and reproductive performance,
evidenced by increased fetal death rate and perinatal mortality,
particularly in the second generation. The nickel deficient rats
were less active during the suckling period, had a rougher hair coat,
and weighed less at weaning. Liver changes were also observed in
nickel deficient rats, as in chicks. Rations low in nickel have also
been developed by Anke and co-workers on which pigs showed a slower
rate of weight gain, delayed sexual maturity, and higher piglet mortality
than controls receiving 10 ppm nickel.
When the mothers of experimental rats were maintained on a nickel
deficient diet, the young, similarly maintained, exhibited a marked
growth inhibition, especially in the second generation. With 15 ppm
nickel in the diet the weight differences at 30 days of age averaged
16% in the F1 generation and 26% in the F2 generation. An adverse effect
on iron absorption resulting in severe anaemia was apparent in the
nickel deficient rats. Iron storage in the liver, spleen, and kidneys
was reduced 87%, 77% and 46% respectively, compared with rats on an
adequate nickel intake.
Selenium Deficiency and Functions
Reproductive Disorders In all species studied, selenium deficiency
results in impaired reproductive performance. The fertility of rats
fed a low selenium, torula yeast diet with adequate vitamin E over
successive generations was severely affected. The animals grew and
reproduced normally but their offspring were almost hairless, grew
slowly, and failed to reproduce. Sterility was determined by lack
of breeding with fertile rats, and in the males, by examining for
spermatozoa. In five of the eight untreated males immotile sperms,
with separation of heads from tails, were observed, with no spermatozoa
in the remaining untreated males. A supplement of 0.1 ppm selenium
as Na2SO3 restored hair coat, growth, and reproductive capabilities.
. Further investigation revealed degenerative changes in the epididymis,
in addition to impaired testicular growth and function, in the rats
fed the selenium deficient diets. Epididymal function probably related
to sperm maturation, appeared to be even more sensitive to selenium
deficiency than the development and functioning of the testis. The
motility of spermatozoa improved almost linearly with increasing
amounts of selenium from 0.01 to 0.08 ppm, added to the basal diet.
A high seasonal incidence of infertility in ewes occurs in parts of
New Zealand. In certain of these areas, 30% of the ewes may be infertile
and losses of lambs are high. The fertility of these ewes is dramatically
increased by selenium administration before mating, and further selenium
treatment reduces the lamb losses.
The infertility results from a high embryonic mortality occurring
between 3 and 4 weeks after conception.
In ewes fed a selenium deficient purified diet satisfactory reproductive
performance was obtained only when selenium and vitamin E were administered
in combination. A combination of selenium and vitamin E injected a
month before mating was similarly shown to improve ewe prolificacy
in selenium deficient areas of Scotland. A sodium selenite-vitamin
E mixture injected into cows a month before calving completely prevented
losses from the birth of premature, weak, or dead calves in part of
California and greatly reduced the incidence of retained placentas
in a herd of cows in Scotland.
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