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ENHANCED MORTALITY AND LIVER DAMAGE IN VIRUS-INFECTED MICE EXPOSED TO PARAXYLENE
Citation:
Selgrade, M., M. Daniels, R. Jaskot, B. Robinson, AND J. Allis. ENHANCED MORTALITY AND LIVER DAMAGE IN VIRUS-INFECTED MICE EXPOSED TO PARAXYLENE. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/047 (NTIS PB94137072), 1993.
Description:
This study assessed effects of p-xylene exposure on mice concurrently infected with murine cytomegalovirus (MCMV). ossible effects included: enhanced infection due to p-xylene induced immune suppression; increased p-xylene toxicity due to viral suppression of cytochrome P-450 (P-450); and additive or synergistic effects on liver function due to tissue injury by both p-xylene and MCMV. ice were exposed to filtered air, 600 or 1200 ppm p-xylene for 6 h/d, for 4 d and infected with a sublethal dose of MCMV after the first exposure. o deaths occurred among uninfected, p-xylene-exposed mice or infected, air-exposed mice, 34% mortality occurred in infected mice exposed to 1200 (but not 600) ppm p-xylene. owever, virus titers in the liver and splenic natural killer cell activity were unaffected by exposure to 1200 ppm p-xylene. mall but significant increases in serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase activities, indicators of liver damage, were observed 4 d post infection. p-Xylene exposure had no effect on these activities in uninfected mice, but 1200 ppm significantly potentiated the effect in infected mice. CMV significantly suppressed and p-xylene significantly increased P-450 levels in the liver but there was no statistically significant interaction between the two. CMV infection suppressed p-nitrophenol hydroxylase, pentoxyresorufin-o-dealkylase, and ethoxyresorufin-o-deethylase activities to a similar degree suggesting that the virus does not preferentially affect specific P-450 isozymes. nhanced mortality in these studies was probably due to enhanced p-xylene toxicity due to suppression of P-450. -Xylene also appeared to potentiate liver damage caused by the virus, although the magnitude of serum enzyme activities indicate that this damage was not sufficient to cause death.