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Biomedical subjects

R S Day

Publications and source records attributed to R S Day.

At least 91 records · Page 5Linked to original sources
PubMed1981

Immunochemical visualization of binding of the chemical carcinogen benzo(a)pyrene diol-epoxide 1 to the genome.

antisera against DNA modified with r-7,t-8-dihydroxy-9,10-oxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE-1) was elicited in rabbits. Such sera reached with either single- or double-stranded modified DNA but not with unmodified DNA, free benzo(a)pyrene, or proteins modified by BPDE-1. Indirect immunofluorescence studies indicated that the immunoglobulin G in the sera bound specifically to the nuclei of KD cells which were treated with BPDE-1. The intensity of fluorescence was proportional to the dose of BPDE-1 used to treat the cells. About 50% of the BPDE-1-DNA adducts remained bound to DNA 24 hr after the removal of the carcinogen. The location of BPDE-1-modified bases in Col E1 DNA was visualized by immunoelectron microscopy.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1980

Defective repair of alkylated DNA by human tumour and SV40-transformed human cell strains.

We have identified a group of 8 (among 39) human tumour cell strains deficient in the ability to support the growth of adenovirus 5 preparations treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but able to support the growth of non-treated adenovirus normally. This deficient behaviour defines the Mer- phenotype. Strains having the Mer- phenotype were found to arise from tumours originating in four different organs. Relative to Mer+ strains, Mer- tumour strains showed greater sensitivity to MNNG-produced killing, greater MNNG-stimulated "DNA repair synthesis and a more rapid MNNG-produced decrease in semi-conservative DNA synthesis. Here we report that (1) Mer- strains are deficient in removing O6-methylguanine (O6-MeG) from their DNA after [Me-14C]MMNG treatment (Table 1); (2) Mer- tumour strains originate from tumours arising in patients having Mer+ normal fibroblasts (Fig. 1a, b); (3) SV40 transformation of (Mer+) human fibroblasts often converts them to Mer- strains (Fig. 1c, d); (4) MNNG produces more sister chromatid exchanges (SCEs) in Mer- than in Mer+ cell strains (Fig. 2).

Adenoviruses, Human↗
PubMed1980

Porphyrins in chronic renal failure.

A highly sensitive thin layer chromatographic assay was used to establish distinct anomalies in hepatic and renal prophyrin synthesis associated with chronic renal failure. Urinary and plasma coproporphyrin disappeared but plasma uroporphyrin (isomer III) levels rose. Patients on maintenance hemodialysis showed elevated red cell protoporphyrin and decreased total stool porphyrins whilst the raised plasma uroporphyrin did not pass into the dialysate, even in 2 cases of overt symptomatic porphyria. These results indicate that urinary coproporphyrin is of renal and not hepatic origin and that azotemia may reduce the activity of the enzyme uroporphyrinogen decarboxylase.

Chromatography, Thin Layer↗
PubMed1979

Familial symptomatic porphyria in South Africa.

Seven members from 3 generations of a family investigated for evidence of symptomatic porphyria (SP) were found to be affected in varying degrees by the disease. Four had cutaneous lesions, while all 7 had biochemical abnormalities diagnostic for SP in their excreta, plasma or hepatic tissue. The results were obtained using the highly sensitive technique of quantitative fluoroscanning after separation of the porphyrin methyl esters by thin-layer chromatography. This clear case of familial SP is rare in South Africa where the high incidence of the sporadic form of the disease is well documented. This study indicates that SP occurs in the following two forms: (i) the sporadic type, usually found as an uncommon associate of chronic liver disease; and (ii) the rare familial type, inherited as an autosomal dominant trait.

Adolescent↗
PubMed1978

Quantitation of red cell porphyrins by fluorescence scanning after thin-layer chromatography.

This paper reports a new method for the quantitative determination of erythrocyte and plasma porphyrins by fluoroscanning of the methyl esters separated by thin-layer chromatography (TLC). After esterification overnight in the dark the polycarboxylated porphyrin methyl esters were extracted into chloroform and aliquots applied to the TLC plates within the range of quantities shown in a preliminary study to be directly proportional to fluorescence intensity. The accuracy and reliability of the technique was tested by comparison of RBC protoporphyrin values obtained by TLC with an established quantitative porphyrin solvent extraction method and with a rapid method presently in common use. Good correlation was demonstrated between the solvent extraction and the TLC techniques. The high sensitivity and adaptability of the TLC technique and its ability to clearly separate all the porphyrins present in the samples are discussed, along with the fluorescence mechanisms involved and the effects of instrumentation.

Chromatography, Thin Layer↗
PubMed1978

Excision repair by human fibroblasts of DNA damaged by r-7, t-8-dihyroxy-t-9,10-oxy-7,8,9,10- tetrahydrobenzo(a)pyrene.

Benzo(a)pyrene diol-epoxide I (r-7,t-8,dihydroxy-t-9,10 oxy-7,8,9,10 tetrahydrobenzo(a)pyrene) was used to treat either human adenovirus 5 or cultures of human fibroblasts. The survival of diol-epoxide I treated adenovirus was greater when infecting fibroblasts from normal persons than when infecting fibroblasts from patients with xeroderma pigmentosum (XP). One diol-epoxide I molecule bound per viral genome correlated with one lethal hit as measured using XP fibroblasts. Normal fibroblasts blocked in semi-conservative DNA synthesis incorporated into their DNA more [3H]thymidine in response to diol-epoxide I treatment than did XP fibroblasts, and also excised more diol-epoxide I from their DNA. All of the effects described above were similar to those obtained when the inactivating agent was ultraviolet light rather than benzo(a)pyrene diol-epoxide I.

Adenoviruses, Human↗