Neoplastic Lesions of Questionable Significance to Humans

Alison, Roger H.; Capen, Charles C.; Prentice, David E.

doi:10.1177/019262339402200211

Cited by 111 publications

(54 citation statements)

References 23 publications

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“…36 This tumorigenic effect of dopamine agonists is peculiar to the rat and considered not to be relevant to human. 37 Leydig cell hyperplasia and tumors in mice are usually associated with estrogenic stimuli. 38,39 Few compounds are associated with necrosis of Leydig cells, the most notable one being ethylene dimethane sulfate.…”

Section: Leydig Cell Changesmentioning

confidence: 99%

Morphologic manifestations of testicular and epididymal toxicity

Vidal¹,

Whitney

2014

Spermatogenesis

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Section: Leydig Cell Changesmentioning

confidence: 99%

Morphologic manifestations of testicular and epididymal toxicity

Vidal¹,

Whitney

2014

Spermatogenesis

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“…The functional effect of PRL on the rat ovary is quite different from that in humans. Whereas PRL directly leads to atrophic corpora lutea or luteolysis in rodents, this does not occur in women [38,39]. Although BRC has been used clinically for therapy in patients with prolactinomas for long-term, there is little information available showing thatt therapeutic BRC affects ovarian and uterine function, and this suggests that the influence observed in the present study may be restricted to the rat.…”

Section: Discussionmentioning

confidence: 60%

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Yoshida

Watanabe

Suzuki

et al. 2009

Journal of Reproduction and Development

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Abstract. The effects of long-term blockade of prolactin (PRL) action by bromocriptine (BRC) treatment on uterine carcinogenesis and on related ovarian physiology were investigated using a rat uterine cancer model. Ten-week-old cycling female Donryu rats, a high yield strain for uterine corpus tumors (endometrial adenocarcinomas), were treated with N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), as a tumor initiator, and injected with 1 mg/kg body weight BRC subcutaneously 4 times per week until 14.5 months of age to block the proestrus PRL surge. The study was terminated at 15 months of age, and the results showed that long-term BRC treatment significantly inhibited endometrial adenocarcinoma development in terms of both incidence (34.6% to 13.0% with significant difference at 5%) and multiplicity (0.35 to 0.18 with significant difference at 5%), which indicates the number of adenocarcinomas per animals. While BRC did not affect estrous cyclicity in the treated animals, a significant decline was evident in the serum 17β-estradiol (E2) to progesterone (P) ratio (E: P ratio), and the serum E2 level showed a decreased tendency at 15 months of age. While the precise pathway to the inhibitory effect could not be determined; the pathway by which ovarian hormonal imbalance decreases the serum E: P ratio most likely plays a crucial role. Key words: Bromocripchne, Long-term treatment, Prolactin blockade, Rat, Uteirne carcinogenesis (J. Reprod. Dev. 55: [105][106][107][108][109] 2009) varian steroidhormone imbalance contributes to uterine carcinogenesis in human beings [1]. Maekawa et al. [2][3][4] have provided evidence that a similar imbalance, especially elevated 17β-estradiol (E2) levels relative to progesterone (P) levels (the E:P ratio), plays a crucial role in promoting endometrial adenocarcinoma development in rodents. While it is well-established that E2 and estrogenic chemicals play supportive or sometimes initiative roles in uterine carcinogenesis in rats as well as women, P may exert an inhibitory influence on human uterine cancer development [5][6][7]. However, the effects of other hormones related to the pituitary or ovaries on uterine carcinogenesis are not well known.Prolactin (PRL) is one of the important regulators of the corpus luteum as well as luteinizing hormone (LH), prostaglandin and vascular endothelial growth factors and platelet derived growth factors in rats [8][9][10]. The function of PRL as a luteotrophic and luteolytic hormone, however, is very complex [11][12][13][14][15][16][17]. Repeated injection of PRL has been shown to stimulate rapid regression of the persistent corpus luteum, with a concomitant decline in total steroidogenic capacity [12,18]. These studies indicate the possibility that the modulation of P production induced by PRL or its inhibitor affect uterine carcinogenesis through ovarian hormonal imbalance. On the other hand, PRL receptors, especially long-form ones (PRLR-L) [19], are present in the uteri of rats. PRL is known to play important roles in adenomyosis formation in ...

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“…That is, estrogens classically inhibit the hypothalamic secretion of dopamine, as a result of which PRL release is stimulated. PRL is luteotrophic in rats; therefore, this also leads to an increase in progesterone 38,39 . On exposure to chronic estrogen or EDCs, the three hormones, PRL, progesterone, and exogenous estrogen, act in synergy, leading to chronic overstimulation of mammary tissue, and then to mammary tumors 38,39 .…”

Section: Caution In the Assessment Of Rat Mammary Glandmentioning

confidence: 99%

“…PRL is luteotrophic in rats; therefore, this also leads to an increase in progesterone 38,39 . On exposure to chronic estrogen or EDCs, the three hormones, PRL, progesterone, and exogenous estrogen, act in synergy, leading to chronic overstimulation of mammary tissue, and then to mammary tumors 38,39 . PRL is not luteotrophic in primates; therefore, this does not occur in woman [38][39][40] .…”

Section: Caution In the Assessment Of Rat Mammary Glandmentioning

confidence: 99%

Endocrine System and Endocrine Disrupting Chemicals(EDCs).

2001

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Abstract:Recently, much has been focused on the potential for a wide range of chemicals to interact with the disruption of the endocrine system in humans and animals. Some of those chemicals have been implicated as endocrine disrupting chemicals (EDCs). We represent this review that the current endocrine systems including of molecular biology and effects of EDCs are discussed, as examples pituitary and mammary gland. Alterations to the endocrine environment caused by EDCs may occur through interference with the synthesis, secretion, transport, binding, action, or elimination of natural hormones responsible for vital homeostasis, differentiation, development, reproduction, and/or behavior. It is important consideration for assessing the adverse effects of EDCs to have an understanding of normal endocrine systems, subsequently, dose, duration of exposure, age, sex, situation, and frequency are estimated. (J Toxicol Pathol 2001; 14: 59-64)

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Neoplastic Lesions of Questionable Significance to Humans

Cited by 111 publications

References 23 publications

Morphologic manifestations of testicular and epididymal toxicity

Morphologic manifestations of testicular and epididymal toxicity

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Endocrine System and Endocrine Disrupting Chemicals(EDCs).

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