Evidence for enhanced secretory function of hepatic macrophages after long‐term ethanol feeding in rats

Yamada, Shinwa; Mochida, Satoshi; Ohno, Akihiko; Hirata, Keiichi; Ogata, Itsuro; Ohta, Yasuhiko; Fujiwara, Kenji

doi:10.1111/j.1600-0676.1991.tb00520.x

Cited by 23 publications

(1 citation statement)

References 14 publications

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“…από in vivo µικροσκοπία δείχνουν ότι τα κύτταρα Kupffer είναι επίσης δυνατόν να φαγοκυτταρώσουν καρκινικά κύτταρα(112). Το µονοξείδιο του αζώτου είναι ένα επιπλέον δραστικό µόριο που παράγεται από τα κύτταρα Kupffer σε απάντηση στην ενδοτοξίνη, τον TNFα, και την προσταγλανδίνη Ε 2 (113) και χρησιµοποιείται από τα Kupffer για την άµυνα έναντι µικροβίων και καρκινικών κυττάρων(114).Χρόνια χορήγηση αιθανόλης τέλος αυξάνει την παραγωγή ελευθέρων ριζών οξυγόνου από τα κύτταρα Kupffer(122). σε πρωτογενή δυσλειτουργία του οργάνου και είναι σηµαντικός επιβαρυντικός παράγοντας στην έκβαση της µεταµόσχευσης(129).…”

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Απομόνωση Και Βιολογική Συμπεριφορά Των Κυττάρων Των Κολποειδών Του Ήπατος

Βαλάτας¹

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Απομόνωση Και Βιολογική Συμπεριφορά Των Κυττάρων Των Κολποειδών Του Ήπατος

Βαλάτας¹

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Inactivation of Kupffer cells prevents early alcohol-induced liver injury

et al. 1994

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It is well recognized that consumption of alcohol leads to liver disease in a dose-dependent manner; however, the exact mechanisms remain unclear. Hypoxia subsequent to a hypermetabolic state may be involved; therefore, when it was observed recently that inactivation of Kupffer cells prevented stimulation of hepatic oxygen uptake by alcohol, the idea that Kupffer cells participate in early events that ultimately lead to alcohol-induced liver disease became a real possibility. The purpose of this study was to test that hypothesis. Male Wistar rats were exposed to ethanol continuously by means of intragastric feeding for up to 4 weeks using the model developed by Tsukamoto and French. In this model, ethanol causes fatty liver, necrosis and inflammation--changes characteristic of alcohol-induced liver disease in human beings. Kupffer cells were inactivated by twice weekly treatment with gadolinium chloride (GdCl3), a selective Kupffer cell toxicant. AST levels were elevated to 192 +/- 13 and 244 +/- 56 IU/L in rats exposed to ethanol for 2 and 4 wk, respectively (control value, 88 +/- 7). This injury was prevented almost completely by GdCl3 treatment. Fatty changes, inflammation and necrosis were also all reduced dramatically by GdCl3 treatment. The average hepatic pathological score of rats treated with ethanol for 4 wk was 4.3 +/- 0.6, which was reduced significantly in ethanol- and GdCl3-treated rats to 1.8 +/- 0.5 (p < 0.05). Rates of ethanol elimination were elevated 2- to 3-fold in rats exposed to ethanol for 2 to 4 wk. This elevation was blocked by GdCl3 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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In situ detection of oxidative stress in rat hepatocytes

Mochida

Masaki

Ohta

et al. 1992

The Journal of Pathology

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In rat hepatocytes in primary culture incubated with nitro blue tetrazolium, formazan content was increased by addition of t-butyl hydroperoxide, a potent oxidant, in a dose-related manner, but not by addition of valinomycin, which kills hepatocytes through mitochondrial damage. This increment after t-butyl hydroperoxide addition was not seen in hepatocytes preincubated with deferoxamine mesylate, a ferric iron chelator which inhibits radical formation. Liver perfusion with nitro blue tetrazolium and t-butyl hydroperoxide in rats produced formazan deposition faintly on the surface of hepatocytes throughout the liver and prominently in the cytoplasm of some hepatocytes, which was attenuated when performed following deferoxamine mesylate perfusion. When liver perfusion with nitro blue tetrazolium was performed in carbon tetrachloride-intoxicated rats, formazan deposition appeared diffusely in hepatocytes in the centrilobular areas. Similar deposition was also observed on the surface and in the cytoplasm of hepatocytes in the periportal and mid-zonal areas in rats undergoing post-ischaemic reperfusion. Liver perfusion with nitro blue tetrazolium can detect in situ oxidative stress in hepatocytes and may be a useful tool for studying the role of lipid peroxidation in rat liver injury.

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Evidence for enhanced secretory function of hepatic macrophages after long‐term ethanol feeding in rats

Cited by 23 publications

References 14 publications

Απομόνωση Και Βιολογική Συμπεριφορά Των Κυττάρων Των Κολποειδών Του Ήπατος

Απομόνωση Και Βιολογική Συμπεριφορά Των Κυττάρων Των Κολποειδών Του Ήπατος

Inactivation of Kupffer cells prevents early alcohol-induced liver injury

In situ detection of oxidative stress in rat hepatocytes

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