On the mechanism of the formation of choleic acids.
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Biomedical subjects
Publications and source records attributed to G Abel.
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Treatment of arg- or strd mutant cells of Chlamydomonas reinhardii with a furocoumarin epoxide, heraclenin, plus UV-A resulted in a decrease in survival and a UV-A dose-dependent increase in induced Arg+ or Strs revertants. Imperatorin, a furocoumarin with a very similar structure but lacking an epoxide group showed a very similar phototoxic and photomutagenic activity in these mutant strains. Treating the mutant cells with heraclenin or imperatorin in the dark neither influenced survival nor mutation induction. The results are discussed with respect to the involvement of the epoxide moiety of heraclenin in mutagenicity.
Heraclenin, a furocoumarin with an epoxide group in its side chain, was analyzed to see if it induced structural chromosome aberrations and sister-chromatid exchanges (SCEs) in human lymphocytes in vitro. The results were compared directly with those of imperatorin, which differs from heraclenin only in lacking an epoxide group. An equally strong clastogenic effect was found for both heraclenin and imperatorin: the number of metaphases with breaks was increased in both cases by approximately a factor of 6. Heraclenin produced a considerable dose-dependent increase in the SCE rate, i.e., by about 60 induced SCEs/metaphase, whereas imperatorin induced only about 4 SCEs/metaphase. The results are discussed with respect to the occurrence of structural aberrations, which are primarily due to the basic furocoumarin structure itself, whereas the large increase in the SCE rate produced by heraclenin is most probably significantly influenced by its epoxide group.
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OBJECTIVE: To determine the prevalence of monoclonal rheumatoid factors (mRF) bearing the WA cross-idiotype (WA XId) in hepatitis C virus (HCV) positive type II mixed cryoglobulins, to review recent studies on the role of HCV in the cutaneous vasculitis lesions in patients with type II cryoglobulinemia and to discuss the implication of these studies for the etiopathogenesis and therapy of the disease. METHODS: Thirty type II cryoglobulins were tested for WA and PO XId and for HCV RNA: RESULTS: WA mRF were strongly, although not exclusively, associated with HCV in type II mixed cryoglobulinemia. CONCLUSION: These and other recent studies from our laboratory suggest that chronic HCV infection may be the stimulus for the production of WA mRF and that HCV may be directly involved in the pathogenesis of the cutaneous vasculitis in patients with type II cryoglobulinemia. The association of HCV infection with the disease provides a rationale for anti-viral therapy and for monitoring therapy by measuring the HCV level in both blood and liver.