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At least 523 records · Page 29Linked to original sources
PubMed1984

Characterization of hepatic DNA damage induced in rats by the pyrrolizidine alkaloid monocrotaline.

Hepatic DNA damage induced by the pyrrolizidine alkaloid monocrotaline was evaluated following i.p. administration to adult male Sprague-Dawley rats. Animals were treated with various doses ranging upward from 5 mg/kg, and hepatic nuclei were isolated 4 hr later. Hepatic nuclei were used as the DNA source in all experiments. DNA damage was characterized by the alkaline elution technique. A mixture of DNA-DNA interstrand cross-links and DNA-protein cross-links was induced. Following an injection of monocrotaline, 30 mg/kg i.p., DNA-DNA interstrand cross-linking reached a maximum within 12 hr or less and thereafter decreased over a protracted period of time. By 96 hr postadministration, the calculated cross-linking factor was no longer statistically different from zero. No evidence for the induction of DNA single-strand breaks was observed, although the presence of small numbers of DNA single-strand breaks could have been masked by the overwhelming predominance of DNA cross-links. These DNA cross-links may be related to the hepatocarcinogenic, hepatotoxic, and/or antimitotic effects of monocrotaline.

Animals↗
PubMed1982

Alkylation of N2 in deoxyguanosine by dehydroretronecine, a carcinogenic metabolite of the pyrrolizidine alkaloid monocrotaline.

Dehydroretronecine, an antimitotic and carcinogenic agent, reacted with deoxyguanosine at pH 7.4 in vitro to yield in nearly equal quantities two major adducts, which were isolated by thin-layer and high-pressure liquid chromatography. The adducts were stable at pH 8.7 and 30 degrees for at least 24 hr, showed pKas at acidic and alkaline pHs, reacted with 4-(p-nitrobenzyl)-pyridine, had a nonexchangeable guan-8-yl proton, and contained equimolar quantities of the pyrrole and nucleoside moieties. From the above data and comparison of proton magnetic resonance spectra of dehydroretronecine, deoxyguanosine, and the adducts, both products were identified as derivatives with a bond between C-7 of dehydrosupinidine and N2 of deoxyguanosine. Mass spectral fragmentation patterns and infrared and ultraviolet absorbance spectra were also consistent with N2 substitution. Circular dichroism spectra established the identities of each of the adducts as 7-(deoxyguanosin-N2-yl)dehydrosupinidine; they are enantiomeric at C-7. These results demonstrate that the reactive electrophile derived from protonated dehydroretronecine readily alkylates the N2-position of deoxyguanosine at C-7 in an SN1 reaction to yield a racemic mixture of products.

Alkylation↗
PubMed1980

Effect of pyrrolizidine alkaloid-induced hepatic disease on plasma amino acid patterns in the horse.

Plasma amino acid patterns were studied in 6 clinically normal adult horses during the course of hepatic disease induced by feeding them plants containing pyrrolizidine alkaloids. At death, there were significant (P less than 0.01) increases in glutamine, proline, tyrosine, asparagine, lysine, histidine, alanine, phenylalanine, methionine, aspartic acid, and ornithine values. There were no significant changes in glycine, valine, isoleucine tryptophan, and arginine values. There were significant (P less than 0.01) decreases in citrulline. Ammonia increased 4-fold. Alpha-Aminoadipic acid and alpha-aminobutyric acid were not detectable in the plasma of clinically normal horses, but were in the plasma of horses with severe hepatic disease. The ratio of branched chain amino acids (isoleucine + leucine + valine) to phenylalanine plus tyrosine progressively decreased from a normal of +/- 0.5 to 1.3 +/- 0.3 (mean +/- SD) just prior to death. The relative changes in plasma amino acid pattern in horses with hepatic diseases seem similar to those changes occurring in man and other animals with hepatic disease.

2-Aminoadipic Acid↗
PubMed1994

Differing embryotoxic effects of senecionine and senecionine-N-oxide on the chick embryo.

The embryotoxic properties of pyrrolizidine alkaloids senecionine (water insoluble) and senecionine-N-oxide (water soluble) were examined using the CHEST method (Chick Embryotoxicity Screening Test). The beginning of the embryotoxicity range for senecionine was found to be between 3-30 micrograms; senecionine-N-oxide, on the other hand, showed no effect even with 100 micrograms dose. On the basis of the theoretical calculation, it can be expected that senecionine embryotoxicity for mammals ranges between 10-100 mg/kg maternal body weight, overlapping in this way the known adult toxicity range. The rat LD50 of most alkaloids known to be significant for human health are in the range of 34-300 mg/kg.

Animals↗