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Biomedical subjects

P Rauko

Publications and source records attributed to P Rauko.

8 recordsLinked to original sources
PubMed1991

Evaluation of synergism of drugs cis-diamminedichloroplatinum (II) and arabinosylcytosine on the level of chemical interaction with DNA and on the growth of mouse leukemia.

1. Cytotoxic synergism of drugs cis-diamminedichloroplatinum(II) (cis-DDP) and arabinosylcytosine (araC) was studied both on the level of interaction with DNA in chemically determined conditions and on leukemia L1210 bearing mice. 2. AraC and its structural natural precursor cytidine were tested for the modulation of kinetics of bifunctional adducts production induced by cis-DDP in DNA. 3. This process plays the basic role in cytotoxic mechanism and antitumor activity of cis-DDP. 4. No interaction was seen between cis-DDP and araC. Further, presence of araC in reaction mixture had no effect on cis-DDP-DNA interaction. 5. Therefore, cytotoxic synergism does not arise in the araC-cis-DDP-DNA interaction and its origin is different. 6. Finding that cytidine has no synergistic effect on life span of leukemia L1210 bearing mice when administered together with cis-DDP it shows the difference between cytidine and araC. 7. The small structural difference between cytidine and araC is very important for synergism of cytotoxicity.

Animals↗
PubMed1990

Electrophoretic analysis of DNA modifications induced by cis- and trans-diamminedichloroplatinum (II) during heat-denaturation of conformation isomers of pBR322 DNA.

The use of conformation isomers of pBR322 DNA in the study of interactions of Pt complexes with DNA provided for a good monitoring of induced changes in the structure of DNA by gel electrophoresis. On the basis of characteristic changes in the gel electrophoretic mobility of platinated isomers of pBR322 DNA we detected the presence of Pt-DNA adducts representing both intra- and interstrand bifunctional binding of Pt complexes to DNA. Also, this method made it possible to distinguish between DNA modifications induced by the therapeutically active cis-diamminedichloroplatinum (II) (cis-DDP) alone, and those induced by its therapeutically inactive trans-isomer (trans-DDP). The electrophoretically detected DNA modifications were more effective if the interaction of the Pt complex took place with heat-denatured DNA. This process, as compared to that performed with native DNA, ran 100 times faster.

Cisplatin↗
PubMed1988

Decrease in intensity of DNA fluorescence caused by interaction between DNA and platinum complexes.

The decrease of DNA fluorescence caused by an impaired capacity of ethidium bromide to intercalate into the DNA reflected structural changes caused in the DNA molecule by its interaction with platinum complexes. This fall in DNA fluorescence was proportional to the length of exposure of DNA to the platinum complexes, and depended on the environment in which the interaction took place. The therapeutically active cisplatinum (cis-DDP) was more efficient to inhibit fluorescence in a solution of 4 X 10(-3) mol NaCl than its therapeutically inactive trans-isomer (trans-DDP). For comparison, the inhibition of DNA fluorescence was also studied in a solution of 10(-2) mol NaClO4. The inhibitory effect was elicited more rapidly, but no difference was found between the two isomers. We concluded that the larger effect of cis-DDP on DNA was induced by the 4 X 10(-3) mol concentration of NaCl. Since also the intracellular concentration of chloride ions is 4 X 10(-3) mol, it cannot be ruled out that the interaction between DNA and cis-DDP and trans-DDP in vivo might be influenced by the intracellular environment.

Chlorides↗
PubMed1976

Thymineless death in a thymine-dependent mutant of Micrococcus radiodurans T2 in the presence of chloramphenicol and rifampicin.

A possibility to prevent cells of a thymine-dependent mutant of Micrococcus radiodurans T2 from thymineless death was investigated. It was found that the presence of chloramphenicol (CAP) in a thymineless medium only decelerated the death of cells. The presence of rifampicin (RFP) considerably decreased the death rate of cells but could not prevent thymineless death completely.

Chloramphenicol↗
PubMed1976

The broth effect and mutation frequency decline in cells of Escherichia coli after irradiation with UV-light.

Dependence of the broth effect and the phenomenon of mutation frequency decline on dose of the applied UV radiation was investigated in the strain Escherichia coli B/r Hcr+ thy trp. Reversions to Trp+ were followed. The degree of the broth effect and the mutation frequency decline is minimal within the range of UV doses corresponding to a survival of cells lower than 10(-1). In connection with the two effects, excision of thymine dimers, initiation of synthesis, synthesis and degradation of DNA were also investigated. It was found that stimulation or inhibition of an inaccurate postreplication repair mechanism, rather than inhibition or stimulation of excision of thymine dimers, are responsible for the broth effect and the mutation frequency decline, respectively.

Culture Media↗
PubMed1976

Role of post-replication and excision repair mechanism in the induction of Trp+ revertants of UV-irradiated Escherichia coli.

Both the post-replication and the excision repair mechanism participate in the induction of Trp+ revertants in Escherichia coli B/r Hcr+ thy trp after a UV-irradiation. At low radiation doses (surviving cell fraction greater than 10(-1) most Trp+ reversions are due to post-replication repair mechanism while at high doses (surviving cell fraction less than 10(-1)) the Trp+ reversions arise probably as the result of an inaccurate excision repair. The absolute accuracy of repair processes decreases with increasing radiation dose.

DNA Repair↗
PubMed1976

Elimination of lethal and pre-mutational DNA lesions during the photoreactivation of UV-irradiated Escherichia coli.

The comparison of the frequency of trp+ revertants of Escherichia coli B/r Hcr+ thy trp after UV-irradiation on the one hand and after UV-irradiation plus photoreactivation on the other showed that both photoreversible pyrimidine dimers of the cyclobutane type and the non-photoreversible DNA lesions cause, at equal lethal effects, also trp+ reversions with the same efficiency. If lethal, the pyrimidine dimers may thus be conceived as primary pre-mutational lesions.

Cyclobutanes↗