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PCBs induce microsomal liver enzymes
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such induction may lead to hepatogenic porphyria and increased
degradation of endogenous steroids in the liver
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PCBs are considered prototypes of workplace chemicals causing
liver toxicity
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liver sensitivity should warn physicians that other organs
may also be affected
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PCBs cause hepatomegaly (enlarged liver), liver hemorrhage,
porphyria and liver damage
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the liver is the major target organ for PCBs
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PCBs produce porphyria
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the liver is the primary target of PCB carcinogenicity
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occupational PCB exposure is associated with subclinical
alterations in serum enzymes suggestive of liver enzyme induction and possible
hepatocellular damage
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PCBs have been responsible for porphyria outbreaks in Turkey
and Japan
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PCBs stimulate drug metabolism and heme synthesis within
1 week of treatment
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PCBs cause hepatic porphyria, weight loss, tremor, liver
damage and increased mortality
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PCBs cause increased accumulation of porphyrins, which causes
hepatic porphyria in different species
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PCBs cause chronic hepatic porphyria
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qualitative changes in urinary porphyrins such as increases
in uroporphyrin and heptacarboxylic-porphyrin, have been noted in PCB exposed
workers
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urinary excretion of porphyrins can be one indicator of PCB
exposure
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PCB caused porphyria, characterized by delayed development,
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PCBs caused increased excretion of urinary uroporphyrins
and accumulation of carboxyporphyrins in the liver
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PCBs increased drug-metabolizing capacity of the liver.
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PCBs caused increased liver weight and porphyria
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PCBs increased all drug metabolizing pathways tested liver
enlargement is observed that may progress to liver damage
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neoplastic liver nodules and hepatocellular carcinomas (liver
cancer)
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porphyria, immunosuppression, and interference with steroid
metabolism, which may be due to increases in microsomal enzyme activity
associated with liver enlargement
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porphyrinogenic PCBs may increase ALA-synthetase by inhibiting
UROD and therefore depleting heme
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hepatic porphyria due to PCBs is the best understood of the
biological effects of this class of compounds
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PCBs cause enzyme induction and inhibition, changes in liver
morphology, hepatic porphyria, and production of liver tumors
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PCBs cause hepatic porphyria
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biotransformation in the liver via hydroxylation and conjugation
with glucuronic-acid, and varying degrees of metabolism and excretion according
to specific molecular structures.
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abnormal findings on liver function tests have been found
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stimulation of enzyme production and porphyria
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PCBs were potent inducers of hepatic porphyria
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Furans had only a slight effect, if any
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hypobilirubinemia in PCB poisoning seems to be caused through
either inhibition of heme catabolism or augmentation of bilirubin elimination
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PCB induces hepatic microsomal enzymes
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PCB induced hypobilirubinemia seems due mainly to accelerated
bilirubin disposal from the blood
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liver enlargement, liver necrosis, and porphyria are some
of the health effects noted in PCB poisoned birds in Green Bay
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liver morphological changes due to PCBs have been studied
extensively.
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a widely studied effect is induction of hepatic microsomal
enzymes in mammals
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PCBs are associated with porphyria
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porphyrins were slightly elevated in children born to PCB-exposed
mothers
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PCBs may damage the cell membrane phospholipid structure
causing the symptoms of porphyria cutanea tarda
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iron greatly sensitizes mice to PCB induced hepatic porphyria
and liver tumor formation
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dietary selenium deprivation may render the livers of rats
more sensitive to PCB effects
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PCBs induce liver enzymes (cytochrome P-450), which increases
the oxidative stress caused by iron, which leads to porphyria.
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PCB-induced uroporphyria may be linked to liver tumors
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PCBs and iron together increase the incidence of porphyria
and liver cancer
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PCB-induced cytochrome P450 (particularly the 1A2 isozyme)
plays a key role in uroporphyria
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ascorbic acid (Vitamin C) prevents uroporphyria
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