Sexual maturation is orchestrated by the central and peripheral actions of the somatotropic and gonadotropic axes along with als from adipose tissue. Alan M. Hoberman, Elise M. Sexual maturation as measured by balanopreputial separation and vaginal patency is evaluated in all rodent studies and can be evaluated in most other species as well.
These landmarks have been demonstrated to be triggered by the presence of reproductive hormones Suckow et al.
Table 7. Chapter 9: Juvenile toxicity study de for the rodent and rabbit. In: Hoberman, A. Body weight on the day of sexual maturation should always be evaluated.
The day of maturation can be altered by substantial changes in growth Diener, Historical control data among laboratories vary as the sex criteria for sexual maturation may vary among laboratories Lewis et al. Renata R. Malcolm K. Jones, in Advances in Parasitology Sexual maturationcompletion of reproductive organs and the maintenance of the female's mature form are dependent on male stimulation Clough, ; Knobloch et al.
Pearce and Huang have suggested that incomplete what maturation may occur due to an absence of endocrine alling from the male. In addition, initiation of mating occurs through the release of a specific pheromone by the male Armstrong, Several studies have shown differences in reproductive organs between unpaired and paired schistosome females in hosts Erasmus, ; Kunz, ; Neves et al. Unpaired females present underdeveloped reproductive organs such as uterus, ovary and ootype, with the vitellarium also not being fully developed Loverde and Chen, Erasmus a demonstrated a decrease in the of eggs passed in the faeces of the host and the presence of disintegrating vitelline cells in the ootype and uterus upon administration of antimony showing that the vitellarium is a candidate target for drugs to treat infection.
Other works have shown similar damage to the vitelline cells using different drugs Erasmus and Popiel, ; Popiel and Erasmus, Neves et al. It was also noted that unpaired females presented undifferentiated vitelline glands containing few vitellocytes. Thomas M. Sexual maturation of cane mice is rapid, and litter sizes are moderately large in comparison with those of other New World muroids such as Peromyscus.
The work of Voss et al.
Females become sexually mature at 21—26 days and males at 40—60 days. Gestation lasts 25 days, with litters usually consisting of four or five young but ranging from 1 to Larger litters consist of smaller neonates, and the young open their eyes at 6—8 days.
By day 16 females wean their young. Ovulation in females is spontaneous.
Pairing females with males in cages divided by wire partitions that permit limited physical contact, but not copulation, does not accelerate the occurrence of estrus or ovulation. Estrous cycling does not differ between single-housed females and females housed with males in divided cages. Copulatory plugs are formed when animals mate.
Pierre C. Sizonenko, in Encyclopedia of Endocrine Diseases Male sexual maturationor puberty, is defined as the period of life during which growth and maturation of the gon named gonadarcheof the internal sex organs, and of the external genitalia occur and the secondary sexual characteristics develop. In addition to these changes, growth velocity is increased in relation to the growth and maturation of the bone cartilage. Simultaneously, psychological and behavioral changes are observed during this period, which is also called adolescence.
In addition, maturation of the adrenal cortex with increased secretion of adrenal androgens termed adrenarche is also noted between the ages of 7 and 9 in boys.
Puberty follows two very important periods in life: 1 sexual differentiation during fetal life and 2 the postnatal surge of gonadotropins and the activation of the hypothalamic—pituitary—gonadal axis, which is observed in male infants between 2 and 6 months of age. Two to 3 years before the onset of the maturation of the gon, the androgenic zone of the adrenal cortex the zona reticularis begins to mature; this may occur at an age as early as 7 years in boys. Adrenal androgens are partially responsible for the development of axillary and pubic hair in boys.
Female sexual maturationor puberty, is defined as the period of life during which growth and maturation of the gon named gonadarcheof the internal sex organs, and of the external genitalia occur and the secondary sexual characteristics sex. In addition, maturation of the adrenal cortex with increased secretion of adrenal androgens termed adrenarche is noted between the ages of 6 and 8 in girls.
Puberty follows two very important periods in life: 1 sexual differentiation during fetal life and 2 the postnatal surge of gonadotropins and the activation of the hypothalamic—pituitary—gonadal axis, which is observed in infants between 2 and 6 months of age, although this activation is less marked than in boys.
Three years before the onset of maturation of the gon, the androgenic zone of the adrenal cortex the zona reticularis begins to mature; this may occur at an age as what as 7 years in girls. Adrenal androgens are responsible for the development of axillary and pubic mature in girls and also contribute ificantly to the development of the labia majora.
Aramandla Ramesh, Anthony E. The sexual maturation and growth of the female vagina, uterus, oviduct, secondary sexual characteristics, breast stromal and ductal development, accelerated bone growth phase and closure of the epiphysis of long bones, growth of ancillary hair and pubic hair, alteration of body fat to produce typical female contours, pigmentation of the nipples and areole, and the genital area are under estrogen regulation.
Hence, a B a P-induced reduction of estrogen secretion at puberty when sexual maturation and growth are expected to occur could delay these processes.
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Furthermore, in addition to the growth effects estrogen has on the uterine and oviductal musculature, it plays a major role in the development of the endometrial lining. Consequently, B a P-induced reduction in estrogen secretion can compromise the ability of the uterus Khorram et al. Because of the near universally accepted theory that oocytes are endowed as a fixed and nonrenewing stockpile at birth Zuckerman and Baker,pathologic destruction of oocytes has been viewed as irreversible. This being the case, the destruction of oocytes by B a P Mattison et al.
Using fish tissues, in vitro studies conducted by Rochas-Montiero et al.
Furthermore, these authors also observed a ificant reduction in the concentrations of conjugated E 2 metabolites in conditioned media, clearly indicating that PAH action in ovary is mediated mainly by the inhibition of steroidogenic enzymes. It is noteworthy that the action of B a P's on the steroidogenic activities in the ovary is not limited to inhibition of estrogen production.
It also enhances the clearance of circulating estrogens. Induction of Ps by PAHs also may lead to an increased metabolism of estrogens as the same P isoforms are involved in estrogen catabolism. These metabolic intermediates initiate toxicity. Therefore, it can be concluded that the repression of estrogen biosynthesis and enhanced metabolism of E 2 by B a P can result in the reduction of the circulating concentrations of this ovarian steroid below physiological threshold essential for maintaining bone and reproductive health.
Even though the toxicity of B a P on various organ systems has been established, not much information is available on their effects on the bone.
Investigations by Naruse et al. Consistent with the findings of Naruse et al. Using in vitro systems, Tsai et al.
To date, only two studies document an association between bone damage and PAH exposure in vivo. Exposure to 3-MC was found to cause a delay in the ossification of the forelimb, hind limb, and cervical and thoracic vertebrae in fetal mice Naruse et al.
Also, exposure to B a P resulted in a loss of bone mature and bone strength in ovariectomized adult rats Lee et al. Thus, there is a clear data gap in the knowledge regarding the mechanisms of bone damage caused by PAHs in an in vivo model. Aramandla Ramesh, Anthony E. Archibong, in Reproductive and Developmental Toxicology The sexual maturation and growth of the female vagina, uterus, oviduct, sex sexual characteristics, breast stromal and ductal development, accelerated bone growth phase and closure of the epiphysis of what bones, growth of ancillary hair and pubic hair, alteration of body fat to produce typical female contours, pigmentation nipples, areolae and the genital area are under estrogen regulation.
Hence a B a P-induced reduction of estrogen secretion at puberty when sexual maturation and growth are expected to occur could delay these processes. Because of the near universally accepted theory that oocytes are endowed as a fixed and non-renewing stockpile at birth Zuckerman and Baker,pathologic destruction of oocytes has been viewed as irreversible.
Exposure to 3-MC was found to cause a delay in the ossification of the forelimb, hindlimb, cervical and thoracic vertebrae in fetal mice Naruse et al. James N. Roemmich, Alan D. Rogol, in Encyclopedia of Endocrine Diseases Growth and sexual maturation are mainly controlled by the growth hormone GH —insulin-like growth factor-1 IGF-1 and hypothalamic—pituitary—gonadal HPG axes.
Many of the growth effects of GH, including long bone growth, are mediated through IGF-1, which is synthesized by target tissues or the liver, the predominant source of circulating IGF IGF-1 also acts as a negative feedback al to reduce GH secretion. Serum IGF-1 concentrations may decline with poor nutrition or chronic illness, opening up the feedback loop and resulting in increased GH secretion but low IGF-1 production.
The net result is relative GH resistance. Increasing estrogen concentrations stimulate a twofold increase in GH secretion that is paralleled by increased serum IGF-1 concentrations. At low concentrations, sex steroids and GH synergistically mediate skeletal growth. At higher concentrations, estrogen induces epiphyseal fusion.
Dennis M. A delay in sexual maturation may be due to chronic disease or malnutrition. This immunological disorder of gluten intolerance produces numerous clinical sequelae, including late puberty, poor growth, delayed menarche, and osteopenia.