Differences in the inhibition of translation by cisplatin, transplatin, and certain related compounds

Sato, Paul H.; Rosenberg, Jeffrey; Sato, Ronald I.

doi:10.1016/s0006-2952(96)00663-6

Cited by 6 publications

(6 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At this 8 hour dose, transplatin's level of toxicity was approximately equivalent to that of 1 µM cisplatin. Similar differences in concentration have been required to achieve equitoxic cisplatin and transplatin doses in other studies (Burczynski et al 2000;Sanchez-Perez et al 1998;Sato et al 1996). Furthermore, this concentration represented the lowest dose at which cytotoxicity levels were relatively low for both drugs.…”

Section: Alamar Blue Tm Cytotoxicity Assayssupporting

confidence: 55%

“…In addition to an equimolar dose of 1 μM, a second approximately equitoxic dose of 25 μM transplatin was also selected for comparison with 1 μM cisplatin. Similar investigations have required transplatin at various doses between 2 and 100 times the concentration of cisplatin to achieve equitoxic effects (Burczynski et al 2000; Sanchez-Perez et al 1998; Sato et al 1996). In addition, at least four-fold more transplatin than cisplatin adducts have been required to significantly inhibit transcription elongation in HeLa cells (Mello et al 1995).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Anti-tumour Agent, Cisplatin, and its Clinically Ineffective Isomer, Transplatin, Produce Unique Gene Expression Profiles in Human Cells

Galea

Murray

2008

Cancer Inform

View full text Add to dashboard Cite

Cisplatin is a DNA-damaging anti-cancer agent that is widely used to treat a range of tumour types. Despite its clinical success, cisplatin treatment is still associated with a number of dose-limiting toxic side effects. The purpose of this study was to clarify the molecular events that are important in the anti-tumour activity of cisplatin, using gene expression profiling techniques. Currently, our incomplete understanding of this drug’s mechanism of action hinders the development of more efficient and less harmful cisplatin-based chemotherapeutics. In this study the effect of cisplatin on gene expression in human foreskin fibroblasts has been investigated using human 19K oligonucleotide microarrays. In addition its clinically inactive isomer, transplatin, was also tested. Dualfluor microarray experiments comparing treated and untreated cells were performed in quadruplicate. Cisplatin treatment was shown to significantly up- or down-regulate a consistent subset of genes. Many of these genes responded similarly to treatment with transplatin, the therapeutically inactive isomer of cisplatin. However, a smaller proportion of these transcripts underwent differential expression changes in response to the two isomers. Some of these genes may constitute part of the DNA damage response induced by cisplatin that is critical for its anti-tumour activity. Ultimately, the identification of gene expression responses unique to clinically active compounds, like cisplatin, could thus greatly benefit the design and development of improved chemotherapeutics.

show abstract

Section: Alamar Blue Tm Cytotoxicity Assayssupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

The Anti-tumour Agent, Cisplatin, and its Clinically Ineffective Isomer, Transplatin, Produce Unique Gene Expression Profiles in Human Cells

Galea

Murray

2008

Cancer Inform

View full text Add to dashboard Cite

show abstract

“…Trans-DDP, administered at the same total dose as cis-DDP, was essentially non-toxic by histological and biochemical assessments (Blisard et al 1991;Mello et al 1995;Sato et al 1996). Thus, Pt contents in the tissue did not correlate with organ damage, which suggest that a mechanism(s) involving steric interactions of Pt species, perhaps with cellular macromolecules such as DNA or RNA, might be important in the differential toxicity of these two compounds.…”

Section: Discussionmentioning

confidence: 96%

Protective Role of Metallothionein on DNA Damage in Rat Kidney Caused by Cis‐Diamminedichloroplatinum

Hosokawa

Okabe

Saito

et al. 2000

Pharmacology & Toxicology

View full text Add to dashboard Cite

Cis-diamminedichloroplatinum (cis-DDP) has been used as an anticancer agent but it also causes nephrotoxicity. To study the cis-DDP metabolism and its effects, the induction of metallothioneins and DNA damage caused by cis-DDP were observed. Cis-DDP or trans-DDP was administered to seven-week-old Wistar male rats as three daily injections of 8.0 mg/kg body wt., intraperitoneally. Using the obtained kidneys, gel filtration assay, metal analysis, immunohistochemistry and terminal deoxy transferase-mediated deoxy uracil triphosphate nick end labeling (TUNEL) method were carried out to examine localization of metallothioneins and DNA damage caused by cis-DDP. Platinum (Pt) contents, 26.05∫12.01 mg/g body wt. and 51.29∫4.59 mg/g body wt. (average∫S.E.) were detected in the kidney of rats injected with both cis-and trans-DDP, respectively. Metallothionein was detected in the cortex of the kidney in rats administrated cis-DDP or trans-DDP. The mRNA was also detected in the same region. On the other hand cis-DDP showed induction of DNA damage on the cells in the outer stripe of the outer medulla but trans-DDP did not show any damage. The regioninduced DNA damage differed from that induced by metallothioneins. Cis-DDP is suggested to be mainly trapped at the proximal tubules by metallothioneins, and the rest of cis-DDP induces DNA damage at the outer stripe of the outer medulla. Metallothioneins are considered to contribute to the protection against cis-DDP in the rat cortex.

show abstract

“…The therapeutic effect is believed to arise as a consequence of cisplatin binding to DNA [3], but it cannot be fully explained solely by this effect because some analogs of cisplatin, including its trans isomer, are not effective anticancer drugs, although they effectively bind to DNA [4]. The difference may lie in the various cellular processings of adducts formed by cisplatin and its analogs [5]. Adducts that are not removed may block DNA replication and transcription.…”

Section: Introductionmentioning

confidence: 99%

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

Błasiak

Kowalik

Małecka‐Panas

et al. 2000

Teratog. Carcinog. Mutagen.

View full text Add to dashboard Cite

Differences in the inhibition of translation by cisplatin, transplatin, and certain related compounds

Cited by 6 publications

References 12 publications

The Anti-tumour Agent, Cisplatin, and its Clinically Ineffective Isomer, Transplatin, Produce Unique Gene Expression Profiles in Human Cells

The Anti-tumour Agent, Cisplatin, and its Clinically Ineffective Isomer, Transplatin, Produce Unique Gene Expression Profiles in Human Cells

Protective Role of Metallothionein on DNA Damage in Rat Kidney Caused by Cis‐Diamminedichloroplatinum

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

Contact Info

Product

Resources

About