Production of Interleukin-6 and Its Implication in Rats after Subcutaneous Injection of Carbon Tetrachloride.

Abstract

Previously, we have reported that interleukin-6 (IL-6) administration reduces hepatic injury caused by carbon tetrachloride (CCl 4 ) and induces the production of antioxidant proteins, manganese superoxide dismutase and metallothionein. In the present study, we examined whether IL-6 was induced endogenously by CCl 4 administration in rats, and examined the relationship between the levels of IL-6 production and hepatic injury. Plasma samples were periodically collected after s.c. administration of 5 ml/kg of CCl 4 (50%, v/v, in corn oil). IL-6 was significantly produced at 1.5 hr after administration, peaked at 8 hr and gradually decreased thereafter. The activities of hepatic marker enzymes, alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) in plasma, gradually increased and peaked at 48 hr. As the ratio of the amount of corn oil to that of carbon tetrachloride was increased in the range of 1 : 0 to 1 : 8 (v/v), IL-6 induction was decreased, while ALT and SDH activities were augmented. When rats were treated with a pharmacological dose of dexamethasone (1 mg/kg), IL-6 production was decreased, but ALT and SDH activities were augmented. IL-6 expression immediately after CCl 4 administration is suggested to play some significant role in reducing hepatic injury. These findings should be thoroughly considered when the hepatic injury model is developed based on the s.c. administration of CCl 4 .

Preventive effect of neutropenia on carbon tetrachloride-induced hepatotoxicity in rats

“…It has been implicated that cytokines such as TNF-α, IL-1, LI-6 and interleukin-10 contribute to liver damage in rats with a single CCl 4 treatment (Czaja et al, 1989(Czaja et al, , 1995DeCicco et al, 1998;Louis et al, 1998;Neubauer et al, 1998;Simeonova et al, 2001;Hojo et al, 2002;Nakamoto et al, 2003;Campo et al, 2004). Edwards et al (1993) have indicated that Kupffer cells cause liver damage in rats with a single CCl 4 treatment possibly by the release of chemoattractants for neutrophils.…”

“…Inflammatory processes in which Kupffer cells, i.e. the resident macrophages of the liver, cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-10, and adhesion molecules such as intercellular adhesion molecule-1 are implicated in the development of CCl 4 -induced acute hepatic injury (Czaja et al, 1989(Czaja et al, , 1995ArmendarizBorunda et al, 1991;Edwards et al, 1993;Tower et al, 1994;DeCicco et al, 1998;Louis et al, 1998;Neubauer et al, 1998;Muriel et al, 2001;Simeonova et al, 2001;Hojo et al, 2002;Nakamoto et al, 2003). It is known that neutrophils, i.e.…”

MODULATION OF INTERLEUKIN-6 AND IMMUNOGLOBULINS IgG AND IgM LEVELS AFTER MULTIPLE ORAL EXPOSURE TO LAMBDA-CYHALOTHRIN IN RATS

“…Opposite to this observation , increased plasma or serum IL-6 level was previously recorded in male rats administered with carbon tetrachloride ( CCl 4 ) either subcutaneously (20) , or orally (21) , or in rats administered orally with the neonicotinoid insecticide acetamiprid (22) .…”

“…Hojo et al, (20) showed that subcutaneous CCl4 administration to rats induced IL-6 production and the level of IL-6 produced seemed to be inversely correlated with the hepatic marker enzymes level in plasma.…”

MRP5b/SMRP mRNA is Highly Expressed in Metallothionein- Deficient Mouse Liver

“…Metallothionein (MT) is a small protein that plays a role in protecting against the toxic effects of heavy metals and xenobiotics as well as in drug resistance and free radical scavenging, [1][2][3][4] and MT knockout mice exhibit hypersensitivity to heavy metals, such as a cadmium 5,6) and mercury. 7) MT is known to be one of the factors involved in resistance to cisplatin, and Sato et al reported that MT knockout mice are more sensitive to cisplatin than normal mice.…”