Anthralin, a non-phorbol tumor promoter, fails to inhibit metabolic cooperation in mutant human fibroblasts, but inhibits phytohemagglutinin-induced lymphocyte blastogenesis in vitro

Toxicology
E C SiG K Yim

Abstract

Two (among many) of the hypotheses put forward to explain mechanisms of action of tumor promoters are: (1) immunosuppression of the host; and (2) inhibition of intercellular junctional communication. Murine spleen cells were exposed for 30 min to various concentrations of anthralin (1,8-dihydroxy-9-anthrone), a polyphenolic non-phorbol promoter, and 1,8-dihydroxyanthraquinone (1,8-DHAQ), an inactive congener. Phytohemagglutinin (PHA)-induced T cell blastogenesis, an indicator of lymphocyte function, was then assessed in vitro. Exposure to anthralin resulted in a concentration-dependent suppression of lymphocyte proliferation with complete suppression occurring at 1 microM. The inactive congener, 1,8-DHAQ, failed to suppress lectin-induced blastogenesis at concentrations up to 10 microM. Dithiothreitol (DTT), a sulfhydryl (SH) compound, failed to protect against the suppression of lymphocyte function by anthralin. In addition, anthralin failed to inhibit in vitro microtubule assembly, a SH-dependent process, in a crude rat brain extract. Finally, unlike 12-O-tetradecanoylphorbol-13-acetate (TPA), the most potent skin tumor promoter known, anthralin failed to inhibit metabolic cooperation between mutant human fibroblasts as assay...Continue Reading

References

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Citations

Oct 24, 2002·Teratogenesis, Carcinogenesis, and Mutagenesis·Timothy J SchraderW Cherry
Jun 1, 1994·Toxicology in Vitro : an International Journal Published in Association with BIBRA·G S BondyC G Rogers
Jul 1, 1992·Journal of the American Academy of Dermatology·H S Zackheim

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