Biomedical subjects

R Rieger

Publications and source records attributed to R Rieger.

93 records · Page 6Linked to original sources

PubMedDate not supplied

Heat-shocks prior to treatment of Vicia faba root-tip meristems with maleic hydrazide or TEM reduce the yield of chromatid aberrations.

Heat-shocks (10 and 30 min at 40 degrees C) prior to treatment with MH or TEM significantly reduced the yield of metaphases with chromatid aberrations. No such effect was observed when ethanol was used for aberration induction. The 'heat-shock effect' on aberration induction by MH and TEM is comparable to 'clastogenic adaptation' observed after pretreatment ('conditioning') with low clastogen concentrations prior to 'challenging' with high clastogen concentrations; both require unimpaired protein synthesis.

Chromosome Aberrations↗

PubMedDate not supplied

Heat shock protection against induction of chromatid aberrations is dependent on the time span between heat shock and clastogen treatment of Vicia faba root tip meristem cells.

Variation of the time span between heat shock (hs) and clastogen treatment of V. faba root tip meristems showed that hs protection is a very quick response (effective after less than 10 min) and lasting for up to 240 min in the case of induction of chromatid aberrations by maleic hydrazide (MH). Analogous protective responses are significantly slower and shorter when TEM is used for aberration induction. This, together with absence of 'clastogenic cross-adaptation' to these agents and differential effects of benzamide (BA, an inhibitor of poly-ADP-ribosylation) pretreatment before hs on hs protection, suggests that hs before clastogen treatment triggers at least 2 clastogen-specific, protective functions which eventually result in protection against these 2 clastogens.

Chromosome Aberrations↗

PubMedDate not supplied

Synthesis of 3,N4-etheno, 3,N4-ethano, and 3-(2-hydroxyethyl) derivatives of 2'-deoxycytidine and their incorporation into oligomeric DNA.

3,N4-Etheno, 3,N4-ethano, and 3-(2-hydroxyethyl)derivatives of 2'-deoxycytidine arise in mammalian DNA that has been exposed to the metabolic products of either vinyl chloride or the antitumor drug bis(chloroethyl)nitrosourea. These chemically-related adducts are thought to be associated with both mutagenesis and carcinogenesis. In this paper we report reliable syntheses of these deoxynucleosides and incorporation of the latter into oligodeoxynucleotides by the phosphoramidite route, using automated methods. It was found that 3-(2-hydroxyethyl)-2'-deoxycytidine is unstable in aqueous solution and undergoes an autoinduced hydrolysis to 3-(2-hydroxyethyl)-2'-deoxyuridine. The rate of this hydrolysis was found to be pH-dependent, having a maximum around pH 8, and a half-life of approximately 5 h. At higher or lower acidities, the reaction rate falls, indicating that the process involves a general acid-base catalysis. Thus in this case, oligomers were obtained that possessed 3-(2-hydroxyethyl)-2'-deoxyuridine residues, rather than the cytidine analogue. It is likely that the former represents the longer-lived species in DNA under physiological conditions. Representative oligomers containing these chemical lesions were analyzed by mass spectrometric and enzymatic degradation methods to confirm their structures.

Base Sequence↗