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Biomedical subjects

R B Webb

Publications and source records attributed to R B Webb.

At least 37 records · Page 2Linked to original sources
PubMed1978

Near-UV mutagenesis: photoreactivation of 365-nm-induced mutational lesions in Escherichia coli WP2s.

Reversion to tryptophan independence induced by 365-nm and 254-nm radiation was studied in Escherichia coli WP2s (B/r trp uvrA). Under aerobic conditions, the mutant frequency responses was of the fluence-square or "two-hit" type at both 365 and 254 nm when revertants were assayed on minimal agar supplemented with 2% nutrient broth (SEM plates). In contrast, when mutants were assayed on minimal agar supplemented with tryptophan only, the revertant yield was reduced to very low values at 365 nm, whereas values substantially greater than with SEM plates were obtained at 254 nm. Premutational lesions induced by both 365-nm and 254-nm radiation were photoreactivated more than 10-fold when assayed on SEM plates, implicating pyrimidine dimers as premutational lesions at both wavelengths. The strong photoreactivation of 365-nm-induced mutagenesis contrasted strikingly with the complete absence of photoreactivation of 365-nm-induced lethality in this strain.

Escherichia coli↗
PubMed1977

Harmful effects of near-ultraviolet radiation used for polymerization of a sealant and a composite resin.

An electronic device used to polymerize a sealant and a composite resin has been found to emit 365-nanometer radiation at levels sufficient to kill the bacterium Escherichia coli rapidly (greater than 14,000 ergs per square millimeter per second). Because of the absence of shielding on the probe, significant amounts of energy (up to 45% of that at the probe tip) were measured at the sides of the probe. These findings--supported by the well-documented findings of biological damage caused by near-ultraviolet radiation, including skin cancer, damage to the lens of the eye, and mutagenic effects--suggest that clinicians take appropriate precautions to avoid potential hazards to themselves and their patients.

Composite Resins↗
PubMed1976

Lethal effects of pyrimidine dimers induced at 365 nm in strains of E. coli differing in repair capability.

Photoreactivation (PR) after 365-nm inactivation was measured in four strains of Escherichia coli differing in repair capability. Photoreactivation was observed in the recA strains K12 AB2480 and K12 AB2463 indicating a significant role of pyrimidine dimers in the lethal action of 365-nm radiation in these strains. Significant PR was not observed in the uvrA strain, K12 AB1886, or in the repair proficient strain, K12 AB1157, after 365-nm inactivation. Biological evidence indicated that stationary phase cells had not lost the capacity for photo-enzymatic repair after fluences of 365-nm radiation of 2 X 10(6) J/m-2 or less. It is proposed that pyrimidine dimers, although induced, are not significant 365-nm lethal lesions in uvrA and wild-type strains because of their efficient dark repair.

DNA Repair↗
PubMed1975

Near-UV photoproduct(s) of L-typtophan: an inhibitor of medium-dependent repair of X-ray-induced single-strand breaks in DNA which also inhibits replication-gap closure in Escherichia coli DNA.

Near-UV photoproducts of L-tryptophan (TP), which are especially toxic for recombination-deficient (rec) mutants, were found to inhibit medium-dependent repair of X-ray-induced single-strand breaks. This inhibitor also slows the rate of closure of replication gaps, suggesting that these two processes may have a common pathway (or share a required step which TP can inhibit).

Centrifugation, Density Gradient↗
PubMed1974

Inhibition of replication gap closure in Escherichia coli by near-ultraviolet light photoproducts of L-tryptophan.

Near-ultraviolet photoproducts of l-tryptophan (TP) differentially inhibited deoxyribonucleic acid (DNA) replication in wild-type cells and uvrA, polA1, and recA recB double mutants of Escherichia coli. Wild-type cells labeled in their DNA with [(3)H]thymidine in the presence of TP produced small pieces of DNA (7 x 10(6) daltons), which corresponded in size to late replicative intermediates of discontinuous DNA synthesis. Moreover, when TP was present, it took five times longer to chase the low-molecular-weight DNA pieces into high-molecular-weight DNA. The observation of replicative intermediates in the presence of TP, and their slow chase into high-molecular-weight DNA in the presence of TP, is strong evidence that TP stabilizes replication gaps in E. coli DNA. Although TP slowed DNA replication in wild-type cells, this effect was transient and DNA synthesis eventually resumed at a normal rate. However, in polA1 and recA recB mutants, DNA synthesis was completely inhibited. Determinations of size and total counts of cells incubated in TP suggested that TP uncouples cell division from DNA replication in recA recB mutants, whereas these processes remain coupled in wild-type cells and in uvrA and polA1 mutants. The slow chase of TP-stabilized pieces of DNA in the presence of TP suggested that the selective effect of TP on DNA synthesis and viability in repair-deficient mutants is a result of TP inhibition of replication gap closure.

Carbon Radioisotopes↗