Mechanisms of in vitro immunosuppression by hepatocyte-generated cyclophosphamide metabolites and 4-hydroperoxycyclophosphamide
References (35)
- et al.
Some studies of the active intermediates formed in the microsomal metabolism of cyclophosphamide and isophosphamide
Biochem Pharmacol
(1974) - et al.
Enhancement of the embryo-toxicity of acrolein, but not phosphoramide mustard, by glutathione depletion in rat embryos in vitro
Biochem Pharmacol
(1987) - et al.
Immunosuppression induced by chemicals requiring metabolic activation in mixed cultures of rat hepatocytes and murine splenocytes
Toxicol Appl Pharmacol
(1986) - et al.
Suppression of in vitro antibody production by dimethylnitrosamine in mixed cultures of mouse primary hepatocytes and mouse splenocytes
Toxicol Appl Pharmacol
(1987) Formation and metabolism of alkylated nucleosides: Possible role in carcinogenesis by nitroso compounds and alkylating agents
Adv Cancer Res
(1977)- et al.
In vitro/in vivo effects of Mesna on the genotoxicity and toxicity of cyclophosphamide—A study aimed at clarifying the mechanism of Mesna's anticarcinogenic activity
Toxicol Lett
(1988) - et al.
Effect of N-acetylcysteine on some aspects of cyclophosphamide-induced toxicity and immunosuppression
Biochem Pharmacol
(1977) - et al.
Differential effects of cyclophosphamide on the B and T cell compartments of adult mice
J Immunol
(1973) - et al.
Selective depletion of lymphoid tissue by cyclophosphamide
Clin Exp Immunol
(1972) - et al.
Studies on the binding of [3H-chloroethyl]-cyclophosphamide and 14[C-4]-cyclophosphamide to hepatic microsomes and native calf thymus DNA
Life Sci
(1977)
A biologically active metabolite of cyclophosphamide
Cancer Res
Studies on the mechanism of action of cytoxan. Evidence of activation in vivo and in vitro
Cancer Res
Formation of the cytotoxic aldehyde acrolein during in vitro degradation of cyclophosphamide
Nature New Biol
Binding of metabolites of cyclophosphamide to DNA in a rat liver microsomal system and in vivo in mice
Cancer Res
Alkylating properties of phosphoramide mustard
Cancer Res
studies on the in vivo formation of acrolein: 3-Hydroxypropylmercapturic acid as an index of cyclophosphamide (NSC-26271) activation
Cancer Treat Rep
Formation, toxicity and inactivation of acrolein during biotransformation of cyclophosphamide as studied in freshly isolated cells from rat liver and kidney
Arch Toxicol
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Molecular docking analyses of Escin as regards cyclophosphamide-induced cardiotoxicity: In vivo and in Silico studies
2021, Toxicology and Applied PharmacologyCitation Excerpt :Research has attributed CPM's toxic effects to its active metabolite, ACR, which interferes with the tissue antioxidant (AO) defense system (Buyukokuroglu et al. 2007; Ağgül et al. 2020) and causes a remarkable proliferation of free radicals (Kawabata et al. 1990; Gür et al. 2020a). Oxidative stress is known to be increased by the number of free oxygen radicals, which, in turn, exposes cell membranes to lipid peroxidation (Kawabata et al. 1990). Likewise, overproduction of free oxygen radicals results in necrosis thanks to the mechanisms including cell and DNA damage, protein denaturation, and peroxidation of membrane lipids (Janero et al. 1991; Cengiz 2018b).
Application of the comparison approach to open TG-GATEs: A useful toxicogenomics tool for detecting modes of action in chemical risk assessment
2018, Food and Chemical ToxicologyCitation Excerpt :Topoisomerase II inhibitors such as ETP, induce DNA double stranded breaks leading to apoptosis through transient stabilization of the topoisomeriase IIα-DNA complex (Choudhury et al., 2004). Also CPA induces DNA strand breaks, however single stranded, through the formation of DNA-DNA crosslinks, leading to inhibition of DNA synthesis and cell apoptosis (Kawabata et al., 1990; Murata et al., 2004). Based on their large overlap in MOA, a match between these two compounds would be expected.
Anticancer system created by acrolein and hydroxyl radical generated in enzymatic oxidation of spermine and other biochemical reactions
2012, Medical HypothesesCitation Excerpt :According to a report by Kawabata and White [75], acrolein was responsible for the enhancement of the, in vitro and in vivo, murine immune responses produced by small doses of CPA [76,77], a phenomenon observed, also, by other workers in animals and humans with cancer [78,79]. In a following study, Kawabata et al. [80] demonstrated, in addition, that acrolein was mainly responsible, at higher dosages, for CPA better known immuno-suppressive activities previously observed, as well, in animals [81] and humans [82]. Acrolein and OH radical, are constantly being generated in normal cell metabolism, and in this communication we are attempting to demonstrate, based on pertinent published data, that together they give rise through a complementation of their effects to a ubiquitous physiological anticancer system.
Oxidative DNA damage induced by a hydroperoxide derivative of cyclophosphamide
2004, Free Radical Biology and Medicine
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Currently in the Department of Biochemistry, Vanderbilt University, Nashville, TN.