 after intravenous administration of bacterial lipopolysaccharide ( lps ) to rats , polymorphonuclear neutrophils ( pmns ) rapidly accumulate in the liver , and midzonal hepatic necrosis is prominent by 6 hr . 
 pmns are required for the development of hepatic injury in rats . 
 certain polychlorinated biphenyls ( pcbs ) can activate pmns , resulting in production of superoxide anion ( o2- . ) and release of cytolytic factors from granules . 
 this raises the possibility that pcb exposure might enhance pmn - mediated tissue injury , such as lps - induced hepatotoxicity . 
 we treated female sprague - dawley rats with a minimally toxic dose of lps in saline ( 2 mg / kg , intravenous ) and 90 min later exposed them to aroclor 1248 ( 50 mg / kg , intraperitoneal ) , a mixture of pcbs . the animals were killed 6 hr after lps administration , and hepatic injury was assessed . 
 neither lps nor aroclor 1248 alone produced liver injury . 
 co - treatment with lps and aroclor 1248 resulted in pronounced liver injury as demonstrated from increased activities of alanine aminotransferase and isocitrate dehydrogenase in plasma . 
 histological evaluation indicated increased severity of hepatic necrosis in rats receiving both lps and aroclor 1248 . 
 hepatic accumulation of pmns , normally observed after lps , was not altered by co - exposure to pcbs . 
 aroclor 1248 stimulated rat pmns in vitro to produce o2- . and to degranulate . 
 in addition , pmn - mediated cytotoxicity to isolated rat hepatocytes in culture was increased upon addition of aroclor 1248 . 
 pcbs activate pmns in vitro and increase pmn - dependent hepatocellular damage in vitro and after lps treatment in vivo . 
 pcbs may act in vivo as an additional inflammatory stimulus to activate pmns to become cytotoxic , resulting in increased tissue injury.imagesfigure 1.figure 2 . 
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 bfigure 5.figure 6 . 
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