Modulation by dimethyl sulphoxide of the toxicity induced by cis-diamminedichloroplatinum in cultured thyrocytes

Massart, Catherine; Tellier, Cindy; Gibassier, J; Leclech, G.; Nicol, M

doi:10.1016/0887-2333(93)90116-m

Cited by 14 publications

(10 citation statements)

References 19 publications

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“…Due to the strong coordination of sulfur at platinum, binding of DMSO at the metal center usually leads to a decrease of the cytotoxic activity of platinum(II) complexes. [22d, f, 30] Steric hindrance of the strongly bound DMSO results in a decreased ability of the DMSO adducts to bind at double-stranded DNA. Therefore, a sample of conjugate 1 was also pre-incubated in DMSO for 24 h prior to dilution with growth medium to form the respective mono-cationic DMSO complex with a chloride counter-ion.…”

Section: Resultsmentioning

confidence: 99%

Conjugation of Cisplatin Analogues and Cyclooxygenase Inhibitors to Overcome Cisplatin Resistance

et al. 2014

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Cyclooxygenase (COX) is an enzyme involved in tumorigenesis and is associated with tumor cell resistance against platinum-based antitumor drugs. Cisplatin analogues were conjugated with COX inhibitors (indomethacin, ibuprofen) to study the synergistic effects that were previously observed in combination treatments. The conjugates ensure concerted transport of both drugs into cells, and subsequent intracellular cleavage enables a dual-action mode. Whereas the platinum(II) complexes showed cytotoxicities similar to those of cisplatin, the platinum(IV) conjugates revealed highly increased cytotoxic activities and were able to completely overcome cisplatin-related resistance. Although some of the complexes are potent COX inhibitors, the conjugates appear to execute their cytotoxic action via COX-independent mechanisms. Instead, the increased lipophilicity and kinetic inertness of the conjugates seem to facilitate cellular accumulation of the platinum drugs and thus improve the efficacy of the antitumor agents. These conjugates are important tools for the elucidation of the direct influence of COX inhibitors on platinum-based anticancer drugs in tumor cells.

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Section: Resultsmentioning

confidence: 99%

Conjugation of Cisplatin Analogues and Cyclooxygenase Inhibitors to Overcome Cisplatin Resistance

et al. 2014

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“…Jones et al demonstrated that co-administration of cisplatin with DMSO in Sprague-Dawley rats reduced nephrotoxicity (48), and Massart and co-workers observed that DMSO inhibited cisplatin cytotoxicity towards cultured thyrocytes while investigating whether DMSO could act as an antidote for cisplatin-induced toxicities, based on previously reported protective effects of DMSO (17). This work was initiated in the context of the desire to utilize known thiols as reactive ‘protective agents’ to temper the side-effects of cisplatin (49).…”

Section: Discussionmentioning

confidence: 99%

“…This renders platinum complexes unstable in DMSO. Massart et al first reported that DMSO reduced cisplatin's cytotoxicity towards cultured thyrocytes (17), and Dernel et al reported that a polymer-based drug delivery system limited activity of cisplatin against stage IIb appendicular osteosarcoma in dogs (18). Little information exists on the effect of DMSO on other platinum drugs and complexes.…”

Section: Introductionmentioning

confidence: 99%

Say No to DMSO: Dimethylsulfoxide Inactivates Cisplatin, Carboplatin, and Other Platinum Complexes

et al. 2014

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The platinum drugs cisplatin, carboplatin and oxaliplatin are highly utilized in the clinic and as a consequence are extensively studied in the laboratory setting. In this study, we examined the literature and found a significant number of studies (11 - 34%) in prominent cancer journals utilizing cisplatin dissolved in dimethylsulfoxide (DMSO). However, dissolving cisplatin in DMSO for laboratory-based studies results in ligand displacement and changes the structure of the complex. We examined the effect of DMSO on platinum complexes, including cisplatin, carboplatin and oxaliplatin, finding that DMSO reacted with the complexes, inhibited their cytotoxicity and their ability to initiate cell death. These results render a substantial portion of the literature on cisplatin uninterpretable. Raising awareness of this significant issue in the cancer biology community is critical, and we make recommendations on appropriate solvation of platinum drugs for research.

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“…Dimethyl sulfoxide (DMSO) can also be used for cisPt dilution, however it is not recommended. The nucleophilic sulphur can displace cisPt ligands, affecting the stability and reducing cisPt cytotoxicity [154]. DMSO introduced in combination studies with cisPt does not affect its activity [152].…”

Section: Compoundsmentioning

confidence: 99%

Common Chemical Inductors of Replication Stress: Focus on Cell‐Based Studies

et al. 2017

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DNA replication is a highly demanding process regarding the energy and material supply and must be precisely regulated, involving multiple cellular feedbacks. The slowing down or stalling of DNA synthesis and/or replication forks is referred to as replication stress (RS). Owing to the complexity and requirements of replication, a plethora of factors may interfere and challenge the genome stability, cell survival or affect the whole organism. This review outlines chemical compounds that are known inducers of RS and commonly used in laboratory research. These compounds act on replication by direct interaction with DNA causing DNA crosslinks and bulky lesions (cisplatin), chemical interference with the metabolism of deoxyribonucleotide triphosphates (hydroxyurea), direct inhibition of the activity of replicative DNA polymerases (aphidicolin) and interference with enzymes dealing with topological DNA stress (camptothecin, etoposide). As a variety of mechanisms can induce RS, the responses of mammalian cells also vary. Here, we review the activity and mechanism of action of these compounds based on recent knowledge, accompanied by examples of induced phenotypes, cellular readouts and commonly used doses.

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Modulation by dimethyl sulphoxide of the toxicity induced by cis-diamminedichloroplatinum in cultured thyrocytes

Cited by 14 publications

References 19 publications

Conjugation of Cisplatin Analogues and Cyclooxygenase Inhibitors to Overcome Cisplatin Resistance

Conjugation of Cisplatin Analogues and Cyclooxygenase Inhibitors to Overcome Cisplatin Resistance

Say No to DMSO: Dimethylsulfoxide Inactivates Cisplatin, Carboplatin, and Other Platinum Complexes

Common Chemical Inductors of Replication Stress: Focus on Cell‐Based Studies

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