Analysis of adaptive response to bleomycin and mitomycin C

Schlade-Bartusiak, Kamilla; Stembalska-Kozłowska, Agnieszka; Bernady, Monika; Kudyba, Marta; Sasiadek, Maria M.

doi:10.1016/s1383-5718(01)00288-1

Cited by 32 publications

(16 citation statements)

References 19 publications

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“…For example, Mahmood et al (1996) reported that in murine cells the AR was induced by the methylating agent methyl methanesulfonate and was stronger than that induced by the ethylating agent ethyl methanesulfonate. Schlade-Bartusiak et al (2002) showed a more pronounced AR in human lymphocytes after treatment with bleomycin, which generates DNA breaks, than with the alkylating agent mitomycin.…”

Section: Molecular Mechanisms Of the Adaptive Responsementioning

confidence: 95%

“…1999; Wang and Cai, 2000;Sawant et al, 2001; Kale, 2001, 2004;Venkat et al, 2001;Assis et al, 2002;Chankova and Bryant, 2002;Gajendiran and Jeevanram, 2002;Rubinelli et al, 2002;Schlade-Bartusiak et al, 2002;Sedgwick and Lindahl, 2002;Jovtchev and Stergios, 2003;Patra et al, 2003;Savina et al, 2003;Ulsh et al, 2004;Zhou et al, 2004;Atanasova et al, 2005;Chankova et al, 2005Chankova et al, , 2007Coleman et al, 2005;Friesner et al, 2005;Lanza et al, 2005;Rohankhedkar et al, 2006;Seo et al, 2006).…”

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confidence: 99%

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Adaptive response: some underlying mechanisms and open questions

2008

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Organisms are affected by different DNA damaging agents naturally present in the environment or released as a result of human activity. Many defense mechanisms have evolved in organisms to minimize genotoxic damage. One of them is induced radioresistance or adaptive response. The adaptive response could be considered as a nonspecific phenomenon in which exposure to minimal stress could result in increased resistance to higher levels of the same or to other types of stress some hours later. A better understanding of the molecular mechanism underlying the adaptive response may lead to an improvement of cancer treatment, risk assessment and risk management strategies, radiation protection, e.g. of astronauts during long-term space flights. In this mini-review we discuss some open questions and the probable underlying mechanisms involved in adaptive response: the transcription of many genes and the activation of numerous signaling pathways that trigger cell defenses -DNA repair systems, induction of proteins synthesis, enhanced detoxification of free radicals and antioxidant production.

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Section: Molecular Mechanisms Of the Adaptive Responsementioning

confidence: 95%

mentioning

confidence: 99%

Adaptive response: some underlying mechanisms and open questions

2008

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“…The AR has been observed in bacteria (Assis et al, 2002;Sedgwick & Lindahl, 2002;Rohankhedkar et al, 2006), yeast (Boreham & Mitchel, 1991;Gajendiran & Jeevanram, 2002), algae (Chankova & Bryant, 2001;Rubinelli et al, 2002;Chankova et al, 2007), insect cells (Savina et al, 2003), mammalian cells (Wang & Cai, 2000;Tiku & Kale, 2001;Ulsh et al, 2004;Zhou et al, 2004), human cells (Schlade-Bartusiak et al, 2002;Atanasova et al, 2005;Coleman et al, 2005;Friesner et al, 2005;Lanza et al, 2005;Seo et al, 2006) and higher plants models (Rieger et al, 1993;Panda et al, 1997;Jovtchev & Stergios, 2003;Patra et al, 2003). A study of the conditions essential for the induction of an adaptive response is of critical importance to understanding the novel biological defense mechanisms against the hazardous effects of radiation.…”

Section: Hormesis and Molecular Mechanisms Of The Adaptive Responsementioning

confidence: 99%

Current Importance and Potential Use of Low Doses of Gamma Radiation in Forest Species

Iglesias-Andreu¹,

Octavio‐Aguilar²,

Bello-Bello³

2012

Gamma Radiation

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“…Three newly established LCLs (each produced by EBV infection of primary B cells from mixed donors and cultured for less than 3 months) were treated with mitomycin C and melphalan, two unrelated drugs that, like cisplatin, are bifunctional alkylating agents and generate DNA cross-links and adducts (6,15). The same LCLs were also treated with the radiomimetic drug bleomycin or the topoisomerase II inhibitor etoposide, which, like ␥-IR, can induce DSBs (but not crosslinks) in DNA (10).…”

mentioning

confidence: 99%

Epstein-Barr Virus Selectively Deregulates DNA Damage Responses in Normal B Cells but Has No Detectable Effect on Regulation of the Tumor Suppressor p53

O’Nions¹,

Turner

Craig

et al. 2006

J Virol

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To determine whether latent Epstein-Barr virus (EBV) modifies DNA damage responses in B lymphocytes, cells were treated with agents either producing DNA cross-links and adducts or generating double-strand breaks. The cyclin-dependent kinase inhibitor p21 WAF1 accumulated in mitogen-stimulated primary B cells following exposure to all genotoxins tested. In contrast, when proliferation was EBV driven, p21 WAF1 failed to accumulate after treatment with the DNA adduct-producing agents. The tumor suppressor p53 was stabilized and phosphorylated after all treatments, irrespective of whether latent EBV was present. This suggests that regulatory pathways upstream of p53 are unaffected by latent EBV but downstream effectors are altered if DNA adducts or distortions are involved.

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Analysis of adaptive response to bleomycin and mitomycin C

Cited by 32 publications

References 19 publications

Adaptive response: some underlying mechanisms and open questions

Adaptive response: some underlying mechanisms and open questions

Current Importance and Potential Use of Low Doses of Gamma Radiation in Forest Species

Epstein-Barr Virus Selectively Deregulates DNA Damage Responses in Normal B Cells but Has No Detectable Effect on Regulation of the Tumor Suppressor p53

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