Polychlorinated biphenyls as inducers of hepatic porphyria in Japanese quail, with special reference to δ-aminolevulinic acid synthetase activity, fluorescence, and residues in the liver

Abstract

Male Japanese quail were orally dosed, daily for 7 days, with 1000, 500, 250, 100, 50, and 0 mg PCB (Aroclor 1260) per kg body weight. The birds receiving 1000 mg/kg died. A dose-related increase in liver and liver: body weight ratio was found. Macroscopic and microscopic examination under ultraviolet light were used for the detection of porphyrin fluorescence. Mitochondrial ALA synthetase activity demonstrated a large increase (20-fold at the 500 mg/kg level; 10-fold at the 50 mg/kg level). The doubling of mitochondrial protein, the increase of ALA synthetase activity, the liver enlargement, and the pyroninophilic staining of the hepatic nucleoli suggest an increased protein synthesis.

In a second experiment, 5 groups of female quail received 100, 10, 1, 0.1, and 0 mg PCB per kg body weight. ALA synthetase activity was increased about 20-fold in the 100 mg/kg group. This increase, together with the high PCB content of the livers (mean 478 ppm) and the incidence of fluorescence, indicating porphyrins, were correlated with the loss of weight in this group (mean 8%). Mobilization of PCB from storage fat is considered to be responsible for the increased porphyria.

The dose-response relationship and liver residue relationship of PCB and ALA synthetase activity are given.