Neuroendocrine Control of Reproductive Function in the Aging Female Rodent

Cooper, Ralph L.; Goldman, Jerome M.; Rehnberg, Georgia L.

doi:10.1111/j.1532-5415.1986.tb04305.x

Cited by 24 publications

(5 citation statements)

References 131 publications

(165 reference statements)

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“…Moreover, exposure to Methoxychlor causes an abnormal LH hormone secretion that was proven histologically to lead to high polycystic follicles and the absence of corpus luteum in the ovary of female rats [ 72 , 73 ]. A previous study also showed that paternally administered Fenvalerate, a pyrethroid insecticide, on male rats indirectly increased the level of testosterone and estradiol-17ß in the rat progeny [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Paternal Fenitrothion Exposures in Rats Causes Sperm DNA Fragmentation in F0 and Histomorphometric Changes in Selected Organs of F1 Generation

Yusoff

Taib

Budin

et al. 2021

Toxics

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The adverse effects of maternal pesticides exposure on the progeny is very well established. However, the impact of paternal exposure to pesticides such as Fenitrothion (FNT) on the histomorphometry of progeny’s organs in unexposed mothers are much less well studied. Therefore, this study aims to evaluate the effects of paternal FNT exposure on the sperm quality of the parent rat and its effects on the histomorphometry of the progeny’s organs. Randomly, male Sprague Dawley rats (n = 24) categorized as F0 were distributed equally into three groups namely Control, FNT-10, and FNT-20. Control received 1 mL/kg corn oil while FNT-10 and FNT-20 received 10 mg/kg and 20 mg/kg of FNT, respectively, via oral force feeding for 28 consecutive days. At the end of the study, male rats were mated with unexposed female rats and the male rats were sacrificed to obtain sperm for sperm characterization and DNA damage evaluation. Meanwhile, the rats’ progeny (F1) namely pControl, pFNT-10, and pFNT-20 were left to grow until postnatal day 70 before being sacrificed to obtain the matured organs for histology and morphometric analysis. Our results showed that both doses of FNT reduced sperm quality and caused DNA fragmentation in F0 rats compared with the control group (p < 0.05). The number of Leydig cells as well as the diameter of the seminiferous tubules and glomerulus of the pFNT-20 group had significantly decreased (p < 0.05) compared with the pControl group. The Bowman’s space of the pFNT-20 group had significantly increased (p < 0.05) compared with the pFNT-10 and pControl groups. Therefore, paternal exposure to FNT reduced the sperm quality and increased sperm DNA fragmentation in F0 male Sprague Dawley rats and altered the histology and morphometry of the selected organs in the F1 progeny.

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Section: Discussionmentioning

confidence: 99%

Paternal Fenitrothion Exposures in Rats Causes Sperm DNA Fragmentation in F0 and Histomorphometric Changes in Selected Organs of F1 Generation

Yusoff

Taib

Budin

et al. 2021

Toxics

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“…Reproductively senescent female rodents have been used to study neuroendocrine changes associated with menopause in women (Cooper et al, 1986;Meites et al, 1980;Wise, 1993Wise, , 1999Wise et al, 1999). This is the first study to report the effects of combined hormone treatment on ischemic RSF rat brain.…”

Section: Discussionmentioning

confidence: 99%

“…Outcome differences may also be a consequence of varying progesterone and estradiol levels in plasma in middle-aged animals versus ovariectomized rats. Most groups characterize RSF rodents in terms of vaginal cytology or gonadotrophin levels (Cooper et al, 1986;LeFevre and McClintock, 1988;Lu et al, 1994;Meites et al, 1980;Wise, 1993Wise, , 1999Wise et al, 1999). Very few groups report hormone levels for RSF rodents.…”

Section: Figmentioning

confidence: 99%

Effects of Combined Estrogen and Progesterone on Brain Infarction in Reproductively Senescent Female Rats

Toung

Chen

Littleton-Kearney

et al. 2004

J Cereb Blood Flow Metab

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Recent data from the Women's Health Initiative have highlighted many fundamental issues about the utility and safety of long-term estrogen use in women. Current hormone replacement therapy for postmenopausal women incorporates progestin with estrogen, but it is uncertain if combined therapy provides major cerebrovascular risks or benefits to these women. No experimental animal stroke studies have examined combined hormone administration. The authors tested the hypothesis that combined hormone treatment reduces ischemic injury in middle-aged female rat brain. Reproductively senescent female rats underwent 2-hour middle cerebral artery occlusion (MCAO) followed by 22 hours reperfusion. Estrogen implants were placed subcutaneously at least 7 days before MCAO, and progesterone intraperitoneal injections were given 30 minutes before MCAO, at initiation, and at 6 hours of reperfusion. Rats received no hormone, a 25-microg estrogen implant, a 25-microg estrogen implant plus 5 mg/kg intraperitoneal progesterone, or 5 mg/kg intraperitoneal progesterone. Cortical, caudoputamen, and total infarct volumes were assessed by 2,3,5-triphenyltetrazolium chloride staining and digital image analysis at 22 hours reperfusion. Cortical and total infarct volumes, except in the acute progesterone-treated group, were significantly attenuated in all estrogen-alone and combined hormone-treated groups. There were no significant differences in caudoputamen infarct volumes in all hormone-treated groups as compared with untreated rats. These data have potential clinical implications relative to stroke for postmenopausal women taking combined hormone replacement therapy.

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“…Many of the effects observed in these studies would suggest that, as in the aging female, the changes in ovarian function in response to atrazine occurred in response to an action of the chlorotriazine on the brain or pituitary. For example, normal reproductive aging is a consequence of an attenuation in the hypothalamic regulation of LH secretion (Cooper et al, 1986). The persistent estrus common in the aging female and in the young, atrazine‐treated female reflect the persistence of unruptured follicles.…”

Section: Mode Of Action Studies: Atrazine Disrupts the Ovulatory Surgmentioning

confidence: 99%

Atrazine and reproductive function: mode and mechanism of action studies

Cooper

Laws

Das

et al. 2007

Birth Defects Research Pt B

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157

102

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Atrazine, a chlorotriazine herbicide, is used to control annual grasses and broadleaf weeds. In this review, we summarize our laboratory's work evaluating the neuroendocrine toxicity of atrazine (and related chlorotriazines) from an historic perspective. We provide the rationale for our work as we have endeavored to determine: 1) the underlying reproductive changes leading to the development of mammary gland tumors in the atrazine-exposed female rat; 2) the cascade of physiological events that are responsible for these changes (i.e., the mode of action for mammary tumors); 3) the potential cellular mechanisms involving adverse effects of atrazine; and 4) the range of reproductive alterations associated with this pesticide.

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Neuroendocrine Control of Reproductive Function in the Aging Female Rodent

Cited by 24 publications

References 131 publications

Paternal Fenitrothion Exposures in Rats Causes Sperm DNA Fragmentation in F0 and Histomorphometric Changes in Selected Organs of F1 Generation

Paternal Fenitrothion Exposures in Rats Causes Sperm DNA Fragmentation in F0 and Histomorphometric Changes in Selected Organs of F1 Generation

Effects of Combined Estrogen and Progesterone on Brain Infarction in Reproductively Senescent Female Rats

Atrazine and reproductive function: mode and mechanism of action studies

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