The antiestrogen toremifene protects against alcoholic liver injury in female rats

Järveläinen, Harri A.; Lukkari, T.A.; Heinaro, S.; Sippel, Helmuth; Lindros, Kai O.

doi:10.1016/s0168-8278(01)00050-2

Cited by 45 publications

(31 citation statements)

References 42 publications

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“…In general, the development of cirrhosis is more common in men than in women (27,39). In contrast, females are more susceptible to alcohol-induced liver injury than are males (40). Although the liver is not a classic sex hormone target, it contains estrogen receptors and responds to estrogen (41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

Protective Role of Estrogen-induced miRNA-29 Expression in Carbon Tetrachloride-induced Mouse Liver Injury

Zhang

Wang

et al. 2012

Journal of Biological Chemistry

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Background: Mechanism underlying the protection of estradiol against CCl 4 -induced hepatic fibrosis remains unclear. Results: miR-29 expression was differentially regulated in male/female mice during CCl 4 treatment. Both estradiol and miR29a/b-expressing adenovirus increased hepatic miR-29a/b levels and attenuated CCl 4 -induced hepatic fibrosis. Conclusion: Estradiol inhibits CCl 4 -induced hepatic injury via inducing miR-29a/b. Significance: Learning the role/regulation of miR-29 in hepatic fibrosis and providing novel therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Protective Role of Estrogen-induced miRNA-29 Expression in Carbon Tetrachloride-induced Mouse Liver Injury

Zhang

Wang

et al. 2012

Journal of Biological Chemistry

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“…16 Current evidence suggests that women develop alcoholic liver disease at lower levels of alcohol intake and throughout a shorter period of time as compared to men, thus making them more susceptible to alcohol-induced liver injury than are males. 17 With regard to the role of sex hormones on disease severity, much of the evidence suggests that the estrogen hormone, which is gender-specific, has a significant influence on disease progression. A significant increase in estradiol levels have been reported in the blood of female patients with alveolitis, histocytosis X, and lung sarcoidosis, with the magnitude of changes in hormone levels correlating with the severity of respiratory failure.…”

mentioning

confidence: 99%

Gender-Based Differences in Bleomycin-Induced Pulmonary Fibrosis

Gharaee−Kermani

Hatano

Nozaki

et al. 2005

The American Journal of Pathology

113

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The role of gender and sex hormones is unclear in host response to lung injury, inflammation, and fibrosis. To examine gender influence on pulmonary fibrosis, male and female rats were given endotracheal injections of either saline or bleomycin. Female rats showed higher mortality rates and more severe fibrosis than did male rats, as indicated by higher levels of lung collagen deposition and fibrogenic cytokine expression. To clarify the potential role of female sex hormones in lung fibrosis, female rats were ovariectomized and treated with either estradiol or vehicle plus endotracheal injections of either saline or bleomycin. The results showed diminished fibrosis in the ovariectomized, bleomycin-treated rats without hormone replacement. Estradiol replacement restored the fibrotic response to that of the intact female mice in terms of lung collagen deposition and cytokine expression, which was accompanied by higher plasma estradiol levels. Furthermore, fibroblasts from bleomycin-treated rats exhibited increased responsiveness to estradiol treatment, causing dose-dependent increases in procollagen 1 and transforming growth factor-␤ 1 mRNA expression relative to untreated controls. Taken together these findings suggest that female mice may have an exaggerated response to lung injury relative to male mice because of female sex hormones, which have direct fibrogenic activity on lung fibroblasts. This may provide a mechanism for a hormonally mediated intensification of pulmonary fibrosis.

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“…This mechanism could be instrumental in induction of higher levels of free oxygen radicals in females after ethanol consumption, which might contribute to increased liver damage. [30] Similarly, in vitro studies showed that there is a difference in enzymatic activities between men and women in alcohol dehdryogenase isoenzyms in the liver. [31] In summary, it is well documented that women are more susceptible to the toxic effects of ethanol than men and develop liver disease earlier and to a higher percentage than men drinking equivalent amounts of alcohol.…”

Section: Mechanisms For Gender Differencesmentioning

confidence: 99%

Liver, Alcohol and Gender

Müller

2006

Wien Med Wochenschr

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Gender differences in alcohol-induced liver injury have been well described. Females develop alcoholic liver injury more rapidly and have a lower alcohol toxic threshold than men. The mechanism for this difference is poorly characterized, differences in first-pass metabolism in the stomach, or elimination rate, or alcohol distribution volume in the body have been suggested. In addition, estrogen has a major influence on the susceptibility of Kupffer cells to gut-derived LPS resulting in increased proinflammatory cytokine production, which could be a major contributing factor to the increased risk of women to alcohol-induced liver disease.

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The antiestrogen toremifene protects against alcoholic liver injury in female rats

Cited by 45 publications

References 42 publications

Protective Role of Estrogen-induced miRNA-29 Expression in Carbon Tetrachloride-induced Mouse Liver Injury

Protective Role of Estrogen-induced miRNA-29 Expression in Carbon Tetrachloride-induced Mouse Liver Injury

Gender-Based Differences in Bleomycin-Induced Pulmonary Fibrosis

Liver, Alcohol and Gender

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