Gadolinium chloride pretreatment ameliorates acute cadmium-induced hepatotoxicity.

Cadmium is a known industrial and environmental pollutant. It causes hepatotoxicity upon acute administration. Features of cadmium-induced acute hepatoxicity encompass necrosis, apoptosis, peliosis and inflammatory infiltration.

Effect of 5-HT(2) receptor blockade on cadmium-induced acute toxicity.

The protective effect of 5-HT(2) receptor blockade with ketanserin or ritanserin against cadmium liver injury was investigated. Male Wistar rats were injected intraperitoneally with a sublethal dose of cadmium (3.5 mg/kg body weight).

Peliosis hepatis: microscopic and macroscopic type, time pattern, and correlation with liver cell apoptosis in a model of toxic liver injury.

Macroscopic and microscopic types of peliosis hepatis, time pattern, and correlation with hepatocyte and sinusoidal cell apoptosis were investigated. Male Wistar rats were injected with a dose of cadmium (6.5 mg CdCl(2)/kg body weight, intraperitoneally; group I).

Effect of serotonin receptor 2 blockage on liver regeneration after partial hepatectomy in the rat liver.

Unlabelled: The effect of serotonin receptor 2 blockade (5-HT(2)) on liver regeneration after 30-34% and 60-70% partial hepatectomy in the rat liver was investigated.

Materials And Methods: Male Wistar rats were subjected to 60-70% (group I) and 30-34% (group II) partial hepatectomy. Serotonin receptor 2 blockade was exerted by intraperitoneal administration of ketanserin at different doses and time points after partial hepatectomy.

The effect of hepatic stimulator substance (HSS) on liver regeneration arrest induced by 5-HT2 receptor blockade.

Background: The restorative effect of hepatic stimulator substance (HSS) against hepatic regeneration arrest induced by 5-HT2 receptor blockade was investigated.

Materials And Methods: Male Wistar rats were subjected to 60-70% partial hepatectomy and to 5-HT2 receptor blockade at 16 h after partial hepatectomy by ketanserin administration (6 mg/kg bodyweight intraperitoneally; group I). HSS at the dose of 100 mg protein/kg bodyweight was administered at 10 or 17 h after partial hepatectomy in ketanserin-treated rats (groups II and III).

The hepatoprotective effect of hepatic stimulator substance (HSS) against liver regeneration arrest induced by acute ethanol intoxication.

Male Wistar rats were randomized to receive ethanol (2.5 ml/kg by gastric intubation every 8 hr; group I), equal volumes of isocaloric to ethanol sucrose solution (group II), or ethanol and HSS (100 mg/kg intraperitoneally 10 and 16 hr after partial hepatectomy; groups III and IV, respectively) for up to 96 hr after partial hepatectomy, with ethanol administration starting 1 hr prior to partial hepatectomy. Animals were killed at 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 60, and 96 hr after partial hepatectomy.

Effect of hepatic stimulator substance (HSS) on cadmium-induced acute hepatotoxicity in the rat liver.

The hepatoprotective effect of HSS against cadmium-induced liver injury was investigated. Rats were intoxicated with a dose of cadmium (3.5 mg/kg b.

Time-course of cadmium-induced acute hepatotoxicity in the rat liver: the role of apoptosis.

Exposure to toxic metals and pollutants is a major environmental problem. Cadmium is a metal causing acute hepatic injury but the mechanism of this phenomenon is poorly understood. In the present study, we investigated the mechanism and time-course of cadmium-induced liver injury in rats, with emphasis being placed on apoptosis in parenchymal and nonparenchymal liver cells.