|1.||Tung, Y M: 1 article (12/2014)|
|2.||Lau, C F: 1 article (12/2014)|
|3.||Loo, C K: 1 article (12/2014)|
|4.||Kan, Y M: 1 article (12/2014)|
|5.||Chan, W C: 1 article (12/2014)|
|6.||Chan, W S: 1 article (12/2014)|
|7.||Brock, W J: 1 article (11/2002)|
|8.||Cappon, G D: 1 article (11/2002)|
|9.||Slauter, R W: 1 article (11/2002)|
|10.||Keller, D A: 1 article (11/2002)|
07/01/2001 - "The present study was initiated after an accidental outbreak of hepatitis in an industrial setting to examine whether concomitant exposure to 2-chloro-1,1,1,2-tetrafluoroethane (HCFC-124), which is not hepatotoxic, could enhance the liver toxicity of HCFC-123. "
12/01/2014 - "We report a cluster of acute hepatitis in five air-conditioning maintenance workers following accidental exposure to 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123). "
07/01/1994 - "Similarities in the response between halothane and HCFC-123 in this guinea pig model suggests that humans susceptible to halothane-induced hepatitis may be susceptible to HCFC-123 by a common mechanism of toxicity."
02/15/1991 - "Because halothane causes an idiosyncratic, and sometimes fatal, hepatitis that is associated with an immune response against several trifluoroacetylated liver proteins, the present findings raise the possibility that humans exposed to HCFC-123 or structurally related HCFCs may be at risk of developing an immunologically mediated hepatitis."
07/01/2001 - "The liver toxicity of HCFC-123 was confirmed by pathological examination of liver tissue, which showed mild (foci of necrotic hepatocytes) to moderate (multifocal random degeneration and necrosis) damage. "
09/01/1995 - "HCFC-123 caused minimal liver injury with only 1 of 8 exposed animals displaying confluent zone 3 necrosis. "
11/01/2002 - "Microscopic evaluation of maternal liver from HCFC-123 exposed animals revealed mild to moderate centrilobular hepatocyte vacuolation, trace to mild centrilobular necrosis, and trace to mild subacute inflammation. "
07/01/1994 - "Lesions related to HCFC-123 and halothane exposure were limited to the liver and included centrolobular vacuolar (fatty) change, multifocal random degeneration and necrosis, and centrolobular degeneration and necrosis. "
|3.||Body Weight (Weight, Body)
11/01/2002 - "These findings demonstrate that HCFC-123 is not a peroxisome proliferator in adult Rhesus monkeys and postnatal exposure to HCFC-123 does not affect body weight of nursing infant monkeys."
11/01/2002 - "Exposure of monkeys to 1000 ppm HCFC-123 did not result in exposure-related clinical observations, or changes in body weight, appetence and behavior. "
08/01/2001 - "Treatment of the mothers with HCFC-123 did not influence milk production based on the body weight difference of the dam before suckling and 60 min after beginning of suckling using 12-pup "standard litters" of untreated dams. "
12/01/1996 - "It was concluded that exposure to HCFC 123 did not cause reproductive effects although it did effect the body weight gain of the offspring during lactation."
|4.||Liver Diseases (Liver Disease)
02/01/1999 - "Acute liver dysfunction among workers exposed to 2,2-dichloro-1,1,1-tryfluoroethane (HCFC-123): a case report."
08/23/1997 - "We investigated an epidemic of liver disease in nine industrial workers who had had repeated accidental exposure to a mixture of 1,1-dichloro-2,2,2-trifluoroethane (HCFC 123) and 1-chloro-1,2,2,2-tetrafluoroethane (HCFC 124). "
|5.||Drug-Induced Liver Injury
|2.||2,2-dichloro-1,1,1-trifluoroethane (HCFC 123)
|4.||Proteins (Proteins, Gene)
|7.||1,1,1,2-tetrafluoro-2-chloroethane (HCFC 124)