Physiological And Biochemical Reviews Of Sex Differences And Carcinogenesis With Particular Reference To The Liver

Yc, To

doi:10.1016/s0065-230x(08)60752-6

Cited by 46 publications

(18 citation statements)

References 375 publications

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“…Spontaneous liver cancer in both humans and animals occurs predominantly in males (14)(15)(16)(17)(18)(19). Also, liver cancer induced in various experimental animal models usually shows a male predominance (14,17), as exemplified by the resistant hepatocyte model (20,21).…”

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“…Also, liver cancer induced in various experimental animal models usually shows a male predominance (14,17), as exemplified by the resistant hepatocyte model (20,21). Several studies have shown that liver cancer formation induced by chemicals in animals can be affected greatly by various hormonal manipulations, such as hypophysectomy and castration, demonstrating the importance of hormones in the carcinogenic process (14,17,(19)(20)(21).…”

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confidence: 99%

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Diethylnitrosamine causes pituitary damage, disturbs hormone levels, and reduces sexual dimorphism of certain liver functions in the rat.

Liao

Blanck

Eneroth

et al. 2001

Environ Health Perspect

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The acute toxicity of diethylnitrosamine (DEN) to the liver has been well documented in the literature, but whether DEN also affects the endocrine parameters has been addressed in only a few studies. We thus investigated the effects of DEN on pituitary, serum hormone levels, and certain sex-differentiated liver enzymes in this study. Adult male Wister rats were intraperitoneally injected with DEN at a single dose of 200 mg/kg and were sacrificed at 1, 3, 7, and 35 days after injection; DEN-treated females were included as controls at days 7 and 35. Electron microscopic observation showed that during the first week after injection, all types of granular cells of the anterior pituitary in male animals exhibited cellular damage, including disrupted organelles and cellular structure, as well as pyknotic or lytic nuclei. Many undamaged secretory cells exhibited dilated endoplasmic reticula, hypertrophic Golgi complexes, and peripheral location of secretory granules, which usually are morphologic features of increased cellular activities. In male rats, the serum level of total testosterone decreased and the corticosterone increased 1 day after DEN treatment. The serum level of growth hormone (GH) decreased and the prolactin level increased on day 3. The hepatic expression of the male-specific cytochrome P450 2C11 (CYP2C11) decreased to 1-5% of the normal levels during the first week and was still 50% lower than the normal level on day 35, whereas the female-specific CYP2C12 expression increased only slightly. Activities of the male predominant 16alpha, 16beta, and 6beta hydroxylation of androstenedione by microsome decreased in an in vitro assay, whereas the non-sex-differentiated 7alpha hydroxylation and the female-predominant 5alpha reduction of androstenedione were unaffected. In female rats, decreased serum GH level was observed on day 7. The CYP2C12 expression in females was decreased to about 1% and 80% of the normal levels on day 7 and day 35, respectively, but the CYP2C11 expression was unchanged. These data suggest that in male rats, DEN treatment may cause pituitary damage, disturb serum hormone levels, and induce long-lasting reduction of sexual dimorphism in certain liver functions.

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confidence: 99%

Diethylnitrosamine causes pituitary damage, disturbs hormone levels, and reduces sexual dimorphism of certain liver functions in the rat.

Liao

Blanck

Eneroth

et al. 2001

Environ Health Perspect

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“…Since 81b; 1989; Moore et al, 1981;Vesselinovitch & oestrogen modulates the secretion of pituitary hormones, ihailovich, 1983). Our previous study (Yamamoto et al, especially prolactin (Toh, 1973;Meites, 1974), the pituitary 91) using both female and male mice treated with 3'-Megland may be involved in the suppressive effects of oestrogen AB neonatally, showed that adenomatous nodules on hepatocellular tumourigenesis. On the other hand, Goldpeared earlier than carcinomas in males, and that the farb and Pugh (1990) have suggested that the promoting arked decrease in incidence of adenomatous nodules in effect of ovariectomy on hepatocellular tumourigenesis in males was accompanied by the marked decrease in mice may be related to weight gain, as ovariectomy results in cidence of carcinomas.…”

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confidence: 95%

“…This sex difference in susceptibility is partly ascribable to the promoting effect of testosterone secreted by the testes after puberty (Vesselinovitch et al, 1980;Moore et al, 1981;Kemp et al, 1989;Weghorst & Klaunig, 1989). The promoting effect of testosterone on hepatocellular tumourigenesis has been studied not only in mice but also in rats, and has been shown to be due to indirect actions of testosterone on tissues other than the liver, such as the thyroid gland, not to a direct action on the liver (Toh, 1973;Kemp et al, 1989). On the other hand, several studies (Vesselinovitch & Mihailovich, 1967;Vesselinovitch et al, 1980;Goldfarb & Pugh, 1990;Yamamoto et al, 1991) have indicated that the ovaries suppress hepatocellular tumourigenesis in mice, ovariectomy after the administration of carcinogens shortening the latency in development of hepatocellular tumours and increasing the incidence of tumours.…”

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Suppression by oestrogen of hepatocellular tumourigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene

Yamamoto

Tatsuta²,

Terada³

1993

Br J Cancer

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Treatment of female C57BL/6 x DS-F1 mice with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) neonatally resulted in the development of adenomatous nodules and glucose-6-phosphatase (G-6-Pase) deficient foci at 8 and 6 months of age, respectively. Ovariectomy of these mice at 1 month of age hastened the development and increased the incidences of these lesions. Subcutaneous implantation of estradiol-17 beta (E2) with ovariectomy at 1 month of age markedly decreased the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 or 12 months of age, but subcutaneous implantation of progesterone did not reduce their incidences. Subcutaneous implantation of E2 into ovariectomised mice at 6 months of age resulted in significant decreases in the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 months of age, but implantation of E2 into the spleen of ovariectomised mice of the same age had no effect on their incidences. The present results suggest that E2 suppresses the development of adenomatous nodules and G-6-Pase deficient foci induced in the mouse liver by 3'-Me-DAB by actions on tissues other than the liver. Images Figure 1

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“…Testosterone treat-a higher frequency and a shorter latency time than ment further decreased CYP2C12 and induced CYP2C11 females. 3,4 Ample animal studies have demonstrated to the level in male liver. Hepatic foci positive for the the importance of androgens for the sex differences, 3,4 placental form of glutathione-S-transferase (GST-P) whereas the role of ovarian hormones is still uncertain.…”

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Persistent sex differences in growth control of early rat liver lesions are programmed during promotion in the resistant hepatocyte model

et al. 1996

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The persistent sex differentiation in focal proliferation The effects of gonadal hormones on several parameand c-myc expression indicated that a hormone-reguters associated with sex-differentiated promotion in the lated change in growth control was introduced during resistant hepatocyte (RH) model were studied. Male and 2-AAF/PH treatment. (HEPATOLOGY 1996;23:835-839.) female rats were initiated with diethylnitrosamine and promoted with 2-acetylaminofluorene (2-AAF) and partial hepatecomy (PH). Before promotion, some femaleThe incidence of liver cancer in many countries is rats were ovariectomized, with or without receiving sub-much higher in men than in women, 1 and female pacutaneous testosterone implants. Rats were killed either tients with liver cancer have been reported to have at the time of cessation of 2-AAF treatment or 2 weeks better survival rates and a lower rate of tumor recurlater. Ovariectomy decreased the messenger RNA rence than male patients. 2 In several experimental sys-(mRNA) expression of the female-specific cytochrome tems using rodents, males develop liver cancer with P450 2C12 (CYP2C12) at the time of PH, but did not increase the male-specific CYP2C11. Testosterone treat-a higher frequency and a shorter latency time than ment further decreased CYP2C12 and induced CYP2C11 females. 3,4 Ample animal studies have demonstrated to the level in male liver. Hepatic foci positive for the the importance of androgens for the sex differences, 3,4 placental form of glutathione-S-transferase (GST-P) whereas the role of ovarian hormones is still uncertain. were larger in male than in female rats. Ovariectomy Estrogen treatment decreases the tumor induction by did not affect the size of foci, whereas testosterone treat-2-acetylaminofluorene (2-AAF) in rats of both sexes 5 ment increased the size to the male level. At the time of and by 2-diacetylaminofluorene in castrated male cessation of 2-AAF treatment, the labeling index, deter-rats. 6 Ovariectomy of female rats increases the tumorimined as cells staining for proliferating cell nuclear antigenicity of 3 -methyl-4-dimethylaminoazobenzene, 7 the gen, was higher in foci of males and testosterone-treated number of preneoplastic nodules induced by 2-AAF, 8 females than in foci from females with or without ovariectomy, whereas the labeling index in the surrounding and the promotive effects of phenobarbital. 9 These data hepatocytes was lower in males and testosterone-treated suggest a protective role of ovarian hormones in hepafemales. Two weeks later, the sex differences in labeling tocarcinogenesis. Other studies indicate that ovariecindex were still present in foci, but no differences were tomy decreases the promotive effects of the carcinogen observed in the surrounding hepatocytes. An elevated c- 2,3,7,8-tetrachlorodibenzo-p-dioxin, 10 to which females myc expression was observed in nodules isolated 3 weeks are more susceptible, and has no effects on tumor inafter PH from males and testosterone-treated females, duction by 2-AAF 8 or 2-diacetylaminof...

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Physiological And Biochemical Reviews Of Sex Differences And Carcinogenesis With Particular Reference To The Liver

Cited by 46 publications

References 375 publications

Diethylnitrosamine causes pituitary damage, disturbs hormone levels, and reduces sexual dimorphism of certain liver functions in the rat.

Diethylnitrosamine causes pituitary damage, disturbs hormone levels, and reduces sexual dimorphism of certain liver functions in the rat.

Suppression by oestrogen of hepatocellular tumourigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene

Persistent sex differences in growth control of early rat liver lesions are programmed during promotion in the resistant hepatocyte model

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