RoleofZincintheAbatement ofHepatocellular Damageand Mortality Incidence inEndotoxemic Rats

yadministered Salmonella typhimurium endotoxin significantly protected ratsagainst toxin-induced mortality andhepatocellular damage. Pretreatment withamountsofzincchlorideranging from0.4to2.0mg/100 g ofbodyweight resulted in80to100% survival compared with10%survival inuntreated control ratsat24h after endotoxin treatment. Zincchloride treatment inexcessof2.0mg/100 g ofbody weight appeared tobetoxic andprovided diminished protection. Incontrast with theprotection obtained withZnIP,intravenously administered zincdidnot provide protection. Theeffectiveness ofZnIPtoenhance survival ifitwas given after endotoxin was greatly diminished as a function oftimeafter endotoxin. Theextent ofhepatocellular damage was assessed atvarious times after endotoxinadministration inZnIP-treated anduntreated ratsbymeasurementof plasma ornithine carbamoyltransferase activity andhistological examination of liver sections. Endotoxin absorption fromtheperitoneal cavity andhepatic uptake were studied byusing 51Cr-labeled endotoxin. ZnIPpretreatment significantly reduced 51Cr-labeled endotoxin content ofblood andliver whencompared tountreated controls, andeffectively prevented endotoxin-induced elevations in plasmaornithine carbamoyltransferase