Compensatory Ovarian Hypertrophy Research Articles

Compensatory Ovarian Hypertrophy after Unilateral Oophorectomy: Evaluation of Ovarian Volumes in Pediatric and Adolescent Populations.

Limited data exist on the morphologic and physiologic effect on the remaining ovary after unilateral oophorectomy, especially in the pediatric population. Our aim is to evaluate ovarian volumes following unilateral oophorectomy to determine whether compensatory ovarian hypertrophy occurs in the remaining contralateral ovary. This was a retrospective chart review of ovarian volume measured on ultrasounds that were completed after unilateral oophorectomy. Postoperative ovarian volumes were compared to established radiologic standards. Large tertiary care academic children's hospital in Atlanta, GA. Female patients less than 21years old who underwent unilateral oophorectomy. Ovarian volumes measured on postoperative ultrasounds. A total of 93 patients met inclusion criteria for this study. Serial ultrasounds were performed in slightly more than half of the patients (n=48, 51.6%), totaling 193 postoperative ovarian volumes. The average age of oophorectomy was 10.8years. Prior to surgery, the majority of patients presented with abdominal pain (n=51, 54.8%) or pelvic mass (n=51, 54.8%), and most (n=77, 82.8%) had benign final pathology. Ovarian volumes were compared to 4 published radiologic ultrasound standards. More than 62.2% of ovarian volumes from girls who had previously had unilateral oophorectomy were larger than age-matched standard ovarian volumes. Ovarian enlargement occurs in the contralateral ovary following unilateral oophorectomy in the pediatric and adolescent population. This supports the concept of compensatory ovarian hypertrophy. This knowledge provides valuable information for interpretation of radiologic images in young female individuals who have undergone oophorectomy, and can assist with counseling on the risk of adnexal complications due to ovarian hypertrophy after unilateral oophorectomy.

122. Compensatory Ovarian Hypertrophy After Unilateral Oophorectomy: Evaluation of Ovarian Volumes in Pediatric and Adolescent Populations

Although infrequent, unilateral oophorectomy is performed in the pediatric and adolescent population for indications including adnexal mass concerning for malignancy, adnexal torsion and infection. Limited data exists on the morphologic and physiologic effects on the remaining ovary after oophorectomy, especially in the pediatric population. Studies have shown compensatory hypertrophy of the remaining single ovary in animal studies and similar findings have been noted in the testis in human boys. Our aim is to evaluate ovarian volumes on ultrasound following unilateral oophorectomy in girls to determine if compensatory ovarian hypertrophy occurs in the remaining contralateral ovary.

Compensatory ovarian hypertrophy after unilateral oophorectomy: evaluation of ovarian volumes in the pediatric and adolescent population

Compensatory ovarian hypertrophy after unilateral oophorectomy: evaluation of ovarian volumes in the pediatric and adolescent population

Anti-Müllerian hormone and ovarian aging in mares.

Anti-Müllerian hormone (AMH) is used as a marker of follicle population numbers and potential fertility in several species including horses but limited data exist across the lifespan. No one has decreased ovarian reserve experimentally to investigate whether a corresponding, quantitative decrease in AMH results. Concentrations of AMH across the lifespan were compiled from 1101 equine females sampled from birth to >33 years of age. Young and old mares (averaging 6 and 19 years) were hemi-ovariectomized and circulating AMH was assessed before and daily thereafter for 15 days. The remaining ovary was removed later and blood was drawn again before and after this second surgery for AMH determination. Polynomial regression analysis and analysis of mares grouped by 5-year intervals of age demonstrated AMH concentrations to be higher in mares aged 5-10 and 10-15 years than 0-5 years of age and lower in mares after 20 years of age. There was high variability in AMH concentrations among neonatal fillies, some of which had concentrations typical of males. Hemi-ovariectomy was followed by a decrease of AMH, almost exactly halving concentrations in intact mares. Concentrations of AMH had returned to intact levels in old mares before complete ovariectomy, as if exhibiting ovarian compensatory hypertrophy, but recovery of AMH was not evident in young mares. AMH may reflect ovarian senescence in mares after 20 years of age but is too variable to do so in the first two decades of life. The ovarian endocrine response to hemi-ovariectomy in mares appears to change with age.

Dynamic changes in oogonial stem cell numbers in mouse ovaries during the reproductive cycle and following hemi-ovariectomy

After the initial report that adult mouse ovaries contain oogonial stem cells (OSCs) (Nature 2004 428:145), several groups have succeeded in purifying these cells for in-depth study (Nat Cell Biol 2009 11:631; Differentiation 2010 79:159; Tilly lab, unpublished). To help delineate factors that influence OSCs in vivo, here we evaluated changes in OSC numbers during the reproductive (estrous) cycle and during compensatory ovarian hypertrophy following hemi-ovariectomy (HO).

Effects of acute unilateral ovariectomy to pre-pubertal rats on steroid hormones secretion and compensatory ovarian responses

In the present study we analyzed the existence of asymmetry in the secretion of steroid hormones in pre-pubertal female rats treated with unilateral ovariectomy (ULO) or unilateral perforation of the abdominal wall (sham-surgery). Treated rats were sacrificed at different times after surgery. Since sham-surgery had an apparent effect on the age of first vaginal estrous (FVE) and serum levels hormone, the results of the sham surgery groups were used to assess the effects of their respective surgery treatment groups. On the day of FVE, compensatory ovulation (CO) and compensatory ovarian hypertrophy (COH) were similar in animals with ULO, regardless of the ovary remaining in situ. In ULO treated animals, progesterone (P4) levels were higher than in animals with sham-surgery one hour after treatment but lower in rats sacrificed at FEV. Left-ULO resulted in lower testosterone (T) concentration 48 and 72 hours after surgery. In rats with Right-ULO lower T concentrations were observed in rats sacrificed one or 72 hours after surgery, and at FVE. ULO (left or right) resulted in lower estradiol (E2) concentrations one or 72 hours after treatment. In rats with Left-ULO, E2 levels were higher 48 hours after surgery and at FVE. Left-ULO resulted in higher levels of follicle stimulating hormone (FSH) five hours after surgery and at FVE. FSH levels were higher in rats with Right-ULO sacrificed on FVE. The present results suggest that in the pre-pubertal rat both ovaries have similar capacities to secrete P4, and that the right ovary has a higher capacity to secrete E2. Taken together, the present results support the idea that the effects of ULO result from the decrease in glandular tissue and changes in the neural information arising from the ovary.

Participation of a pure neuronal mechanism in the control of gonadal functions.

The present review summarizes the data on the existence of a neural connection between the gonads and the central nervous system. As an experimental model the development of compensatory ovarian hypertrophy following unilateral ovariectomy was studied. Unilateral ovariectomy or orchidectomy resulted in a higher cellular activity in the hypothalamic arcuate neurons contralateral to hemigonadectomy and an increased luteinizing hormone-releasing hormone content in the medio-basal hypothalamus ipsilateral to the removed gonad. Local treatment of the remaining ovary with 6-hydroxy-dopamine prevented the development of compensatory ovarian hypertrophy after unilateral ovariectomy. Hemitransection of the spinal cord contralateral to hemigonadectomy, different unilateral hypothalamic deafferentations of the medio-basal hypothalamus as well as unilateral lesion of the medial preoptic area or of the arcuate nucleus blocked the compensatory ovarian growth when the brain surgery was on the same side as ovariectomy. Furthermore, in hypophysectomized + unilaterally ovariectomized rats a less severe ovarian atrophy occurred than in animals solely with hypophysectomy. All these data favour the view that - besides the hormonal control - a pure neuronal mechanism is also involved in the regulation of gonadal functions.

Perinatal exposure of female rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces central precocious puberty in the offspring

Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during the fetal and neonatal periods has been indicated to alter the development of the offspring later in life. In this study, we determined whether perinatal exposure to a low dose of TCDD affects the onset of puberty in the female offspring of Long-Evans hooded rats. On day 15 of gestation, pregnant female rats were administered TCDD by gavage at a single dose of 0 (vehicle), 200, or 800 ng/kg b.w. In the female offspring born to dams administered with TCDD at either 200 or 800 ng/kg b.w., the vaginal opening and first estrus occurred approximately 4-7 days earlier than in the offspring born to vehicle-treated animals. The ovarian weight gain was also accelerated following exposure to TCDD in a dose-dependent manner. We next examined the ovarian compensatory hypertrophy (OCH) as an indicator of the maturation of the LH/GnRH-generating system in the pituitary and the hypothalamus. Exposure to TCDD accelerated the onset of OCH in the female offspring in a dose-dependent manner. In particular, in the offspring born to the dams exposed to TCDD at 800 ng/kg b.w., hypertrophy, which is characterized by hyperovulation and a marked increase in the weight of the remaining ovary after hemi-ovariectomy, was observed on postnatal days 27-30, which was 10 days earlier than in the offspring born to the vehicle-treated dams. These results indicate that perinatal exposure to a low dose of TCDD induces precocious puberty, including early maturation of the hypothalamic-pituitary axis, the gonads and genitals, in female Long-Evans hooded rats.

Ipsilateral vagotomy to unilaterally ovariectomized pre-pubertal rats modifies compensatory ovarian responses

The present study evaluates the participation of the vagus nerve in pre-pubertal rats with unilateral ovariectomy on puberty onset, and on progesterone, testosterone and estradiol serum levels, and the compensatory responses of the ovary. Unilateral vagotomy did not modify the onset of puberty in unilaterally ovariectomized rats. Ovulation rates of animals with the left vagus nerve sectioned and the left ovary in-situ was lower than in rats with only unilateral ovariectomy. Sectioning the left vagus to 32-day old rats with the left ovary in-situ resulted in lower compensatory ovarian hypertrophy than in rats with right unilateral ovariectomy. Twenty-eight or 32-day old animals with sectioning of the right vagus nerve and the right ovary in situ showed higher compensatory ovulation. Twenty-eight -day old rats with the right ovary in situ had higher progesterone and testosterone levels than animals of the same age with the left ovary in-situ. Compared to animals with the right ovary in situ, animals treated at 32-days of age, sectioning the ipsi-lateral vagus nerve resulted in higher progesterone levels. Higher progesterone levels were observed in 28- and 32 days old rats with the left ovary in situ and left vagus nerve sectioned. Thirty-two day old animals with the right ovary in situ and right vagus nerve sectioned had higher progesterone levels than rats of the same age with the left ovary in situ and left vagus nerve sectioned. Left vagotomy to 28-day old rats with the left ovary in situ resulted in higher testosterone levels, a reverse response to that observed in animals with sectioning of the right vagus and the right ovary in situ. Thirty-two day old rats with the left ovary in situ and left vagus nerve sectioned showed lower testosterone levels than animals without vagotomy and with the left ovary in situ.Twenty-eight -day old animals with the left vagus sectioned and left ovary in situ had lower estradiol serum levels than rats without unilateral vagotomy, a response similar to that observed in 32-day old rats with the right ovary in situ and right vagus nerve sectioned.Present results suggest an asymmetric regulation of steroid hormones secretion by the vagus nerve innervations in animals with unilateral ovariectomy, and those differences in testosterone serum levels observed are associated to the ovary remaining in-situ, vagal innervation and age when the animals were treated.

Involvement of the peripheral cholinergic muscarinic system in the compensatory ovarian hypertrophy in the rat.

In the present experiments, unilateral ovariectomy (ULO) induced compensatory hypertrophy (COH) of the remaining rat ovary (60%-85% increase in ovarian weight, total proteins, and total RNA and DNA). An increased thymidine uptake preceded the organ enlargement. COH was inhibited by i.p.-administered muscarinic antagonist propantheline (dose-dependently) or botulinum toxin delivered locally to the ovary. The effects were reversed by bethanecol i.p. (a muscarinic agonist). In sham ULO animals, [3H]-scopolamine binding to ovarian membranes indicated the existence of muscarinic receptors (Kd 2.5 nM, Bmax 12 fmol/mg proteins, Hill 1.0). The ovarian 1,2-diacylglycerol (DAG) was 120-150 pmol/mg tissue and did not react to carbachol in vitro (50 microM). At 15 minutes after ULO, the [3H]-scopolamine binding was unchanged (Kd 2.6 nM, Bmax 12.6 fmol/mg tissue, Hill 1.0), but the ovarian DAG was increased (280-350 pmol/mg tissue) and increased further in response to carbachol (460-550 pmol/mg tissue). After ULO, ovarian DAG remained continuously responsive to carbachol. The ULO-induced DAG increase and enhanced susceptibility to carbachol were inhibited by the botulinum toxin or atropine pretreatments. Abdominal vagotomy done immediately before ULO also inhibited the ULO-induced DAG increase and DAG responsiveness to carbachol. However, when the vagotomy was performed 10 mins after ULO, the ovarian DAG remained responsive to carbachol in vitro. The data suggest that the peripheral cholinergic system, including the ovarian muscarinic receptors, stimulates COH. This is apparently associated with the ULO-induced coupling of the ovarian muscarinic receptors to phosphoinositide (PI) breakdown. Vagus plays a role in the occurrence of the changed muscarinic receptor-PI breakdown relationship in the remaining ovary.

Effects of Capsaicin Treatment on the Regulation of Ovarian Compensatory Hypertrophy and Compensatory Ovulation

The present study investigates the effects of functional sensorial denervation, induced by administering capsaicin to hemiovariectomized adult female rats in each day of the estrus cycle, on ovulation and serum concentrations of estrogen and progesterone. The results indicate that the establishment of compensatory ovarian hypertrophy (COH) and compensatory ovulation (CO) depends on both the day of the estrous cycle when sensorial denervation was performed and on which ovary was extirpated. These results support the now accepted notion that the response of the ovaries to denervation is asymmetrical. The results seem to suggest that this asymmetric response is mediated by some specific neu-ral information that is registered in the ovary and sent to the CNS, that such information plays a role modulating the reactivity of the ovarian compartments to gonadotropins, and that the frequency of this signal varies along the estrus cycle.

Temporal effect of carbofuran on estrous cycle compensatory ovarian hypertrophy and follicles in hemiovariectomized albino mice

Carbofuran, a systemic N-methyl carbamate pesticide was administered orally with an effective dose of 1.3 mg/kg per day to hemiovariectomized (HOVX) mice for 5, 10, and 15 days. Sham-operated and HOVX control mice were administered a similar quantity of olive oil. The vaginal smear and body weight of the mice were recorded daily and mice were sacrificed on day 16. The results of the present study indicate that there is a significant decrease in the duration of the estrus with a concomitant significant increase in the duration of the diestrus with carbofuran treatment for 10 days. In the HOVX mice treated with carbofuran for 15 days there was a significant decrease in the length of the estrous cycle and the duration of the estrus and metestrus with a concomitant significant increase in the diestrus. There was a significant increase in the ovarian weight in HOVX control mice when compared to that of the sham operated control mice. HOVX mice treated with carbofuran for 10 and 15 days showed a significant decrease in the relative ovarian weight with a concomitant inhibition of compensatory ovarian hypertrophy in HOVX mice. There was also a significant decrease in the ovarian growth rate in relation to the contralateral ovary of the same animal. There was a significant decrease in the number of small and total number of healthy follicles with a concomitant significant increase in the number of medium, large and total number of atretic follicles in HOVX mice treated with carbofuran for 10 days. There was a significant decrease in the number of small, medium, large, and total number of healthy follicles with a concomitant significant increase in the number of medium, large, and total number of atretic follicles in HOVX mice treated with carbofuran for 15 days. The administration of carbofuran in the present study showed that there is no significant change in the body and organs weight such as uterus, kidney, adrenals, liver, spleen, thymus and thyroid in all the carbofuran-treated mice. The above findings such as disruption in the estrous cycle, inhibition of compensatory ovarian hypertrophy, and follicular toxicity may be due to a direct effect on the ovary or through the hypothalamo–hypophysial–ovarian axis.

Effect of edifenphos on compensatory ovarian hypertrophy, follicular kinetics and estrous cycle in hemicastrated rats.

Edifenphos, an organophosphate fungicide, was administered to hemicastrated albino rats intraperitoneally for 15 consecutive days in graded doses of 2 to 8 mg/kg body weight. In the oil-treated hemicastrated control group, ovarian weight and total number of healthy and atretic follicles were significantly higher than the same parameters in sham-operated control animals, and the estrous cycle was normal. Treatment with 2, 4, 6, or 8 mg/kg/d edifenphos significantly decreased ovarian weight (-6.75, -9.79, -18.71, and -34.13 percent, respectively) below that of the controls. Although treatment with 2 or 4 mg/kg/d edifenphos did not change the number of healthy and atretic follicles, a dosage of 4 mg/kg/d significantly decreased the number and duration of estrous cycles. Treatment with 6 or 8 mg/kg/d, however, significantly decreased the number and duration of different phases of the estrous cycle as well. In all treated groups, the weights of the thymus and uterus were significantly reduced when compared with those of hemicastrated oil-treated control animals.

Effect of endosulfan on ovarian compensatory hypertrophy in hemicastrated albino mice

Endosulfan, a chlorinated cyclodiene insecticide, was administered orally at 1.5, 3, 6, and 9 mg/kg per day to normal hemicastrated virgin mice for 15 consecutive days to examine the effect on ovarian function. Sham-operated and hemicastrated control mice were administered a similar volume of olive oil. The vaginal smear and body weight of the mice were recorded daily and mice were sacrificed on day 16. The remaining left ovary, uterus, kidney, adrenal, liver, thymus, and thyroid were removed and weighed. The left ovary from each animal was serially sectioned and stained for histologic studies. The hemicastrated control mice had a 40.5% increase in weight of the remaining left ovary and a significant increase in healthy and atretic follicles when compared with sham-operated controls. The remaining left ovaries of mice treated with 1.5 mg endosulfan had a 37.2% increase in weight with no significant difference in ovarian weight and or in the healthy and atretic follicles when compared with hemicastrated olive oil-treated controls. However, treatment with 3, 6, and 9 mg endosulfan resulted in weight increases in the remaining left ovary of only 14.9, 7.4, and 0.8% and a significant decrease in healthy follicles with a concomitant increase in the number of atretic follicles compared to the olive oil-treated controls. There was no significant change in the number of estrous cycles or the duration of each phase of the estrous cycle with 1.5 and 3 mg/kg per day endosulfan. However, there was a significant decrease in the number of estrous cycles, and the duration of estrus and metestrus with a concomitant significant increase in the duration of the diestrus phase with 6 and 9 mg/kg per day endosulfan treatment when compared with hemicastrated olive oil-treated controls. There were no significant change in body weight or the weights of the uterus, kidney, adrenal, liver, thymus, or thyroid after endosulfan treatment. These observations show that endosulfan treatment caused a significant decrease in compensatory ovarian hypertrophy. An increase in the number of atretic follicles and disruption of the estrous cycle may have been due to a direct effect on the ovary or to effects on the hypothalamo–hypophysial–ovarian axis.

Effect of dimethoate administration schedules on compensatory ovarian hypertrophy, follicular dynamics, and estrous cycle in hemicastrated mice.

Dimethoate, a widely used organophosphate insecticide, was administered orally (28 mg/kg body weight) to hemicastrated (HC) virgin mice on day 1 and for 5, 10, and 15 days. Hemicastrated untreated control mice showed a significant increase in relative ovarian weight, with 42.74% hypertrophy and an increase in healthy and atretic follicles when compared with those of sham-operated control animals. The HC mice treated for 1 day or for 5 days showed no significant change in ovarian weight (36.64% and 25.19% hypertrophy, respectively) or in healthy and atretic follicles, when compared with HC-control mice. Treatment with dimethoate for 10 or 15 days, however, resulted in a significant decrease in ovarian weight (19.84% and 0.76% hypertrophy, respectively), a significant decrease in the number of healthy follicles, and a concomitant significant increase in the number of atretic follicles when compared with those in HC control animals. No significant change occurred in the number of estrous cycles or duration of each phase of the estrous cycle in HC mice treated with dimethoate for either 1 or 5 days. In HC mice treated with dimethoate for 10 or 15 days, however, a significant decrease in the number of estrous cycles, duration of proestrus, estrus, and metestrus, a concomitant significant increase in the diestrus phase, when compared with HC control animals. In mice receiving dimethoate for 15 days (but not for 1, 5, or 10 days) a significant decrease occurred in body weight and in the weights of the uterus, kidney, spleen, and liver when compared with the parallel weights in HC control animals. The overall findings suggest that following dimethoate treatment, a significant decrease in ovarian weight with a concomitant increase in compensatory ovarian hypertrophy and in the number of healthy follicles, with a concomitant increase in the number of atretic follicles and interrupted estrous cycles, may be due to the direct effect on the ovary or may be due to a hormonal imbalance in any stage of the hypothalamo-hypophysial ovarian axis.

Effects of sympathetic denervation on follicular distribution, oestradiol and progesterone serum levels in prepubertal hemi-ovariectomized female guinea pig

Hemi-gonadectomy performed in prepubertal female guinea pigs is followed by a compensatory ovarian hypertrophy (COH) and compensatory ovulation (CO). Sympathetic denervation diminished the COH (left ovary: 28±1.6% versus 46±4% (control), P<0.05; and right ovary: 21.3±3.2% versus 34.2±3.7% (control), P<0.01) and does not modify the CO. The mean follicular diameter increased only in the right ovary of hemi-gonadectomized animals. This increase is greater in the hemi-gonadectomized-denervated groups. The mean follicular diameter measured in the right and left ovaries showed an opposite response in hemi-ovariectomized and hemi-ovariectomized-denervated animals: the diameter increased in the right ovary without modifications in the left. Present results add further support to the participation of ovarian innervation on the mechanisms, which regulate follicular development.

Effects of guanethidine administration on compensatory ovarian hypertrophy, compensatory ovulation and follicular development in the prepubertal female guinea pig

We analyzed the participation of sympathetic ovarian innervation in the prepubertal female guinea pig on regulation of compensatory ovarian hypertrophy (COH) and compensatory ovulation at puberty. The COH of the left ovary was significantly higher that of the right one (left ovary: 41.5±5.2 vs. 27.5±5.6%, p<0.05, Kruskal–Wallis test). The sympathetic denervation induced by guanethidine administration beginnings at birth or on day 10 resulted in a significant increase of the COH by each ovary ( p<0.05, Kruskal–Wallis test). Only one of the six untreated control guinea pigs sacrificed at the follicular phase ovulate. All the hemiovariectomized animals with the left ovary in situ ovulated, while only two out of five with the right ovary in situ did (100 vs. 40%: p<0.001, Kruskal–Wallis test), unlike the denervated animals, which did not ovulate. The number of corpora lutea present in the ovaries was similar among all groups of animals. These results demonstrate differences in the follicular diameter in untreated female guinea pigs and add further support to the concept of asymmetrical response of the ovaries to denervation.

Effect of mancozeb on ovarian compensatory hypertrophy and biochemical constituents in hemicastrated albino rat ☆

Mancozeb a carbamate fungicide was administered orally at doses of 500, 600, 700, and 800 mg/kg/day to normal hemicastrated virgin rats for 15 consecutive days to examine the effect on ovarian hypertrophy. Sham-operated and hemicastrated control rats were administered a similar quantity of olive oil. The vaginal smear and body weight of the rats were recorded daily and rats were sacrificed on the Day 16. The ovary, uterus, kidney, adrenal, spleen, liver, lungs, heart, thymus, and thyroid were removed and weighed. The left ovary from each animal was serially sectioned and stained for histologic studies. The hemicastrated control rats revealed a significant increase in relative ovarian weight with 66.3% hypertrophy. Treatment with 700 and 800 mg/kg/day mancozeb revealed a decrease in ovarian hypertrophy with 28.2 and 22.8% hypertrophy, respectively. There was no significant change in the number of estrous cycles and duration of each phase of the estrous cycle with 500 mg/kg/day mancozeb. However, there was a decrease in the number of estrous cycles, duration of proestrus, estrus, and metestrus with concomitant significant increase in the duration of the diestrus phase with 600, 700, and 800 mg/kg/day mancozeb treatment. There was a significant decrease in the number of healthy follicles with concomitant increase in the number of atretic follicles at higher doses of mancozeb. There were no significant changes in the body and organ weight with 500, 600, 700, and 800 mg/kg/day of mancozeb. The levels of protein, glycogen, total lipid, phospholipid, and neutral lipid were elevated in the liver, uterus, and ovary after hemicastration. Protein, glycogen, total lipid, phospholipid, and neutral lipid were not significantly changed in the liver, uterus, and ovary after 500 mg/kg/day mancozeb. However, treatment with 600, 700, and 800 mg/kg/day mancozeb showed a significant decrease in the levels of protein, glycogen, total lipid, phospholipid, and neutral lipid in the liver, uterus, and ovary, with the exception of liver total lipid and uterine glycogen. In addition to the decrease in the compensatory ovarian hypertrophy, mancozeb treatment reduced the number of healthy follicles with a concomitant increase in the number of atretic follicles. This finding plus disruption of the estrous cycle may be due to a direct effect on the ovary or the hypothalamo–hypophysial–ovarian axis.

Temporal effect of methyl parathion on ovarian compensatory hypertrophy, follicular dynamics and estrous cycle in hemicastrated albino rats.

Methyl parathion, an organophosphorus pesticide, was administered i.p. at a dose of 5 mg/kg body weight to hemicastrated virgin rats for 1, 5, 10 and 15 days. Treatment with methyl parathion for 1 and 5 days revealed no change in the ovarian weight with -0.64% and -9.63% hypertrophy respectively and no change in healthy and atretic follicles when compared with hemicastrated oil-treated controls. However, treatment with methyl parathion for 10 and 15 days resulted in a significant decrease in ovarian weight gain with -21.36% and -31.98% hypertrophy, respectively, a significant decrease in the number of healthy follicles, and no change in the number of atretic follicles. The number of estrous cycles and duration of each phase of the estrous cycle were significantly affected with methyl parathion treatment for 5, 10 and 15 days. However, there were no significant changes in the number of estrous cycles and duration of estrus and metestrus phases in 1 day methyl parathion treatment except for a decrease and increase in proestrus and diestrus phases respectively. The weight of the uterus was significantly decreased whereas those of the liver, kidney and adrenal did not change in any of the methyl parathion treated groups.

Inhibition of ovarian compensatory hypertrophy by the administration of methyl parathion in hemicastrated albino rats

Methyl parathion, an organophosphorus pesticide that is a potent acetylcholinesterase inhibitor in animals, was administered IP in graded doses from 2.5 to 5.0 mg/kg body weight to normal hemicastrated virgin rats for 15 consecutive days. Sham-operated and hemicastrated control groups were treated with a similar quantity of olive oil vehicle. The vaginal smears and body weights of treated and control groups were recorded daily and rats were sacrified on the 16th day. The ovaries, adrenals, liver, kidney, and uterus were removed and weighed, and the ovary from each animal was serially sectioned and stained for histologic studies. The hemicastrated control group revealed a significant increase in ovarian weight with 45% hypertrophy and a significant increase of total healthy and atretic follicles when compared with sham-operated control rats. Treatment with 2.5 and 3.5 mg methyl parathion revealed no change in the ovarian weight with 48 and 42% hypertrophy, respectively, and no change in healthy and atretic follicles when compared with hemicastrated oil-treated controls. However, treatment with 4.0 and 5.0 mg methyl parathion resulted in a significant decrease in ovarian weight gain with 13 and 8% hypertrophy, respectively, a significant decrease in the number of healthy follicles, and no change in the atretic follicles. The number of estrous cycles and duration of each estrous cycle were affected significantly with 3.5, 4.0, and 5.0 mg methyl parathion treatment when compared with controls. There were no significant changes in adrenal, liver, kidney, or uterine weight in the methyl parathion-treated groups except a decrease in uterine weight with 5.0 mg treatment when compared with oil-treated hemicastrated controls.