Erratum to Amifostine: A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential as a radioprotector and cytotoxic chemoprotector

Spencer, Caroline M.; Goa, Karen L.

doi:10.1007/bf03259124

Cited by 113 publications

(137 citation statements)

References 110 publications

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“…We found no information in the literature about the specific chemoprotective action of MEA against genotoxic chemical products such as alkylating agents. We suggest that the chemoprotection observed here for MEA was due to radical scavenging and hydrogen donation reactions, as reported for the chemoprotective agent WR-1065, the active metabolite of amifostine (Spencer and Goa, 1995). Mazur and Blawat (1999), reported that amifostine significantly reduced MNPCE frequencies in PCE even when administered half an hour before CP.…”

Section: Discussionsupporting

confidence: 79%

“…Mazur and Blawat (1999), reported that amifostine significantly reduced MNPCE frequencies in PCE even when administered half an hour before CP. Spencer and Goa (1995), reported cell protection when amifostine was administered up to one hour after CP therapy. With respect to MEA, we observed a significant reduction in MNPCE frequency even when this aminothiol was administered 30 min before or 30 min after the alkylating agents.…”

Section: Discussionmentioning

confidence: 99%

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Chemoprotective effect of cysteamine against the induction of micronuclei by methyl methanesulfonate and cyclophosphamide

et al. 2005

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Cysteamine or 2-mercaptoethylamine (MEA) is an aminothiol with a well-known radioprotective action. No specific information is available in the literature about the possible chemoprotective action of MEA against genotoxic chemical agents. This paper presents the results of studies on the ability of MEA to protect mouse bone marrow polychromatic erythrocytes against the induction of micronuclei by alkylating agents such as methyl methanesulfonate (MMS) and cyclophosphamide (CP). We observed that MEA administered intraperitoneally 30 min before or 30 min after the administration of MMS or CP significantly reduced the frequency of micronucleated polychromatic erythrocytes (MNPCEs) induced by the alkylating agents. When MEA was administered in combination with MMS or CP the reduction in the frequency of MNPCEs did not reach statistically significant levels, although it reached values close to significance. With respect to the polychromatic erythrocyte/normochromatic erythrocyte (PCE/NCE) ratio, we observed that MEA did not provide significant protection against the bone marrow toxicity induced by CP.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Chemoprotective effect of cysteamine against the induction of micronuclei by methyl methanesulfonate and cyclophosphamide

et al. 2005

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“…Paclitaxel (Ptx) is one of the most effective naturally occurring antineoplastic drugs discovered in recent decades (Spencer and Faulds, 1994). The drug interacts with tubulin dimers in the G2 phase of the mitotic cell cycle to promote microtubule polymerization; the resulting formation of highly stable microtubules prevents cell division and accounts for the cytotoxic properties of Ptx (Singh et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

In vivo efficacy of paclitaxel-loaded injectable in situ-forming gel against subcutaneous tumor growth

Lee

Kim

Kang

et al. 2010

International Journal of Pharmaceutics

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“…However, the platelet anti-aggregant effect occurred at concentrations higher than those causing thrombocytopenia in humans, concentrations at which functional platelet abnormalities have not been observed (Balduini et al, 1992). Other biological effects of anagrelide include a decrease in peripheral vascular resistance and a positive inotropic effect (Spencer & Brogden, 1994). The corresponding clinical manifestations in humans have included postural hypotension, fluid retention, peripheral oedema, and heart palpitations (Anagrelide Study Group, 1992).…”

mentioning

confidence: 99%

The effects of anagrelide on human megakaryocytopoiesis

Solberg

Tefferi²,

Oles³

et al. 1997

Br J Haematol

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Summary.Anagrelide, an inhibitor of platelet aggregation, decreases the number of platelets in normal subjects and in patients with myeloproliferative disorders. We describe studies aimed at discovering the general mechanism(s) by which anagrelide acts. We examined three hypotheses:(1) anagrelide shortens platelet survival, (2) anagrelide inhibits the proliferation of megakaryocytic-committed progenitor cells (CFU-M), and (3) anagrelide inhibits maturation of megakaryocytes. We observed that anagrelide did not shorten platelet survival. Proliferation of CFU-M in vivo was not affected by anagrelide, although high concentrations of anagrelide inhibited CFU-M in vitro. In-vivo and in-vitro anagrelide altered the maturation of megakaryocytes, causing a decrease in their size and changing other morphometric features. We conclude that anagrelide decreases the number of platelets primarily by interfering with the maturation of megakaryocytes.

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Erratum to Amifostine: A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential as a radioprotector and cytotoxic chemoprotector

Cited by 113 publications

References 110 publications

Chemoprotective effect of cysteamine against the induction of micronuclei by methyl methanesulfonate and cyclophosphamide

Chemoprotective effect of cysteamine against the induction of micronuclei by methyl methanesulfonate and cyclophosphamide

In vivo efficacy of paclitaxel-loaded injectable in situ-forming gel against subcutaneous tumor growth

The effects of anagrelide on human megakaryocytopoiesis

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