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PubMed1995

A cytochrome P4502B form is the major bioactivation enzyme for the pyrrolizidine alkaloid senecionine in guinea pig.

1. We have purified three P450s from the liver of the phenobarbital (PB)-treated guinea pig in order to evaluate the role of these enzymes in pyrrolizidine alkaloid (PA) metabolism. 2. PB treatment of guinea pig increased the hepatic microsomal conversion of the PA senecionine (SN) to the pyrrolic metabolite (+/-)6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP), an activation product, and SN N-oxide, a detoxification product by 224 and 70% respectively. 3. Reconstitution of a PB-inducible guinea pig P4502B isoform (M(r) = 57,512 by MALDI-TOF mass spectrometry) in a reconstituted system metabolized SN to DHP and SN N-oxide at rates of 1.98 and 1.45 min-1 respectively. A second purified guinea pig P450, a 2C-type isoform (M(r) = 56,496 by MALDI-TOF mass spectrometry), produced SN N-oxide from SN at the rate of 13.3 min-1 but catalyzed little DHP formation. The third guinea pig P450, an apparent 3A type (M(r) = 54-56,000 by SDS-PAGE), lost its catalytic activity towards SN during the final purification process. 4. Immunoinhibition of microsomal SN metabolism by rabbit antibodies raised against the guinea pig P4502B, 2C and 3A isoforms indicated that the 2B played the most important role (> 70% of the total metabolism) in bioactivation of SN in both the untreated or PB-treated guinea pig, whereas 2C and 3A seemed to exhibit little (around 13%) PA metabolism. P4502B, along with flavin-containing monooxygenase, also contributed to the detoxification of SN in both the untreated (34%) and PB-treated (40%) guinea pig. 5. This study suggests that the putative P4502B form plays the most important role in SN bioactivation in guinea pig.

Amino Acid Sequence↗
PubMed1983

Abnormal alveolar cells in monocrotaline induced pulmonary hypertension.

Monocrotaline given to rats causes lung injury which is followed by pulmonary hypertension. A large, abnormal intraalveolar cell has been repeatedly observed. The purpose of the present study was to define the nature of the cell and to determine how it related to the lung injury. As observed by electron microscopy, the intraalveolar cell contained numerous large, dense granules, as well as lipid whorls, extensive Golgi complexes, and many small vesicles. These cells appeared to be macrophages, possibly altered by ingestion of lipid-like material which was free in the alveolar space. Enlarged type II pneumonocytes and mast cells were seen in the alveolar walls but their appearance differed from that of the free alveolar cells. The electron microscopic findings plus the presence of Fc and C3b receptors on the cells indicated they were alveolar macrophages. When the severity of pulmonary hypertension was varied by a) giving monocrotaline to rats of varying age, b) by varying the dose of monocrotaline, or c) by varying the time interval after monocrotaline administration, the number of abnormal alveolar macrophages related to the severity of the pulmonary hypertension. When we reduced the number of circulating leukocytes by whole body radiation, monocrotaline administration was followed both by accelerated pulmonary hypertension and increased numbers of abnormal alveolar macrophages. The abnormal macrophage appeared to be a marker of the monocrotaline induced pulmonary hypertension. However, neither the abnormal macrophage nor the monocrotaline injury appeared to depend on circulating leukocytes.

Animals↗
PubMed1985

Monocrotaline-induced pulmonary fibrosis in rats: amelioration by captopril and penicillamine.

The purpose of this study was to determine whether Captopril (an angiotensin converting enzyme inhibitor) or D-penicillamine (an inhibitor of collagen crosslinking) can ameliorate pulmonary fibrosis induced by the plant alkaloid monocrotaline. Rats were randomly assigned to one of six treatment groups: (1) control; (2) Captopril, 60 mg/kg/day, p.o.; (3) D-penicillamine, 30 mg/kg/day, p.o.; (4) monocrotaline, 2.4 mg/kg/day, p.o.; (5) monocrotaline plus Captopril, as above; (6) monocrotaline plus penicillamine, as above; and were killed after 6 weeks of continuous drug administration. Monocrotaline-treated rats exhibited several anatomic correlates of pulmonary hypertension, including cardiomegaly, right heart enlargement, and muscularization of the pulmonary arteries and arterioles. These monocrotaline reactions were accompanied by decreased lung activities of angiotensin converting enzyme (ACE) and plasminogen activator (PLA), indicative of endothelial dysfunction; and by increased lung hydroxyproline concentration, indicative of interstitial fibrosis. The presence of interstitial fibrosis was confirmed by electron microscopy. When given concomitantly with monocrotaline, both Captopril and penicillamine partially prevented the cardiomegaly, right heart enlargement, and vascular muscularization. Both agents also diminished the decreased lung PLA activity and increased hydroxyproline concentration observed in monocrotaline-treated animals. Neither modifying agent influenced the monocrotaline-induced decrease in lung ACE activity. Compared with control rats, the rats receiving Captopril alone exhibited decreased heart weight and increased serum ACE activity, and animals receiving penicillamine alone did not differ significantly from control animals for any of the endpoints studied. These data demonstrate that Captopril and penicillamine ameliorate monocrotaline-induced pulmonary fibrosis in rats. Penicillamine, known to inhibit radiation-induced lung injury, thus is shown to be effective in a second model of pulmonary fibrosis. Perhaps more importantly, the hydroxyproline data demonstrate that the ACE inhibitor Captropril exhibits antifibrotic activity in monocrotaline-treated rat lung.

Animals↗
PubMed1999

Ragwort poisoning.

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Agricultural Workers' Diseases↗
PubMed2000

Tansy ragwort poisoning in a horse in southern Ontario.

Bizarre behavior, apparent lameness, and colic were noticed in 1 of 3 horses on a pasture overgrown by weeds during a drought. Liver failure and hepatoencephalopathy were diagnosed, caused by pyrrolizidine alkaloid toxicosis associated with consumption of tansy ragwort. The horse made a full recovery when removed from the pasture.

Animals↗