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Biomedical subjects

C Kidson

Publications and source records attributed to C Kidson.

At least 145 records · Page 8Linked to original sources
PubMed1976

DNA replication and post-replication repair in U.V.-sensitive mouse neuroblastoma cells.

Mouse neuroblastoma cells differentiate when grown in the absence of serum; differentiation is reversed on the addition of serum. Differentiated cells are more sensitive to U.V.-radiation than proliferating cells. Whereas addition of serum to differentiated neuroblastoma cells normally results in immediate, synchronous entry into S phase, irradiation just before the addition of serum results in a long delay in the onset of DNA replication. During this lag period, incorporated 3H-thymidine appears in the light density region of CsCl gradientss, reflecting either repair synthesis or abortive replication. Post-replication repair (gap-filling) was found to be present in proliferating cells and at certain times in differentiated cells. It is suggested that the sensitivity of differentiated neuroblastoma cells to U.V.-radiation may be due to ineffective post-replication repair or to deficiencies in more than one repair mechanism, with reduction in repair capacity beyond a critical threshold.

Cell Differentiation↗
PubMed1976

Repair of ultraviolet light-induced damage in Micrococcus radiophilus, an extremely resistant microorganism.

Repair of ultraviolet radiation damage was examined in an extremely radioresistant organism, Micrococcus radiophilus. Measurement of the number of thymine-containing dimers formed as a function of ultraviolet dose suggests that the ability of this organism to withstand high doses of ultraviolet radiation (20,000 ergs/mm2) is not related to protective screening by pigments. M. radiophilus carries out a rapid excision of thymine dimers at doses of ultraviolet light up to 10,000 ergs/mm2. Synthesis of deoxyribonucleic acid is reduced after irradiation, but after removal of photodamage the rate approaches that in unirradiated cells. A comparison is drawn with Micrococcus luteus and M. radiodurans. We conclude that the extremely high resistance to ultraviolet irradiation in M. radiophilus is at least partly due to the presence of an efficient excision repair system.

Cell-Free System↗
PubMed1976

Resistance of human melanoma cells to ultraviolet radiation.

A series of five human melanoma cell lines has been demonstrated to be highly resistant to ultraviolet (UV) radiation, with a D0 of 400 ergs/sq mm. Melanotic melanoma cells were found to increase their production of melanin following UV radiation, whereas some amelanotic cells did not. Melanotic and amelanotic melanoma cell lines exhibited the same UV resistance; melanoma and nonmelanoma cells formed the same numbers of thymine dimers at a given UV dose. These data imply that melanin does not play a major role in protecting DNA of melanoma cells against UV damage in culture. The rates of removal of thymine dimers from DNA of melanoma cells were comparable to those in UV-sensitive, nonmelanoma cell lines, so that rapid excision repair does not explain UV resistnace in the melanoma cells. No DNA strand breakage was detected in a melanoma cell line at moderate UV doses.

Cell Line↗
PubMed1975

DNA chain termination by 2',3'-dideoxythymidine in replicating mammalian cells.

The thymidine analog, 2,3-dideoxythymidine (ddT), is rapidly phosphorylated and incorporated terminally at 3-ends of growing DNA chains in replicating mammalian cells. Following some initial loss of ddT incorporated into DNA chains, the major portion is retained for periods equivalent to more than two normal cell generations. Some ddT appears at the termini of oligonucleotides, a portion of which have chromatographic properties suggesting internally complementary sequences. While these oligonucleotides may include degraduation fragments, it is possible that some represent replication initiation sequences.

Animals↗
PubMed1975

A repressible DNA-repair system in mouse neuroblastoma cells.

Differentiated mouse neuroblastoma cells are extremely sensitive to UV light even through they can undergo excision-repair. A postreplication repair system present in proliferating cells is reversibly repressed in differentiated neuroblasts, and its genetic control is not coupled directly with DNA replication.

Cell Line↗
PubMed1975

DNA repair and UV resistance in human melanoma.

Human melanoma cells are highly resistant to 254-nm light. Resistance appears to depend on their ability to continue replication after high UV doses due to the presence of a very efficient postreplication repair system, while excision-repair is of relatively minor importance.

Cells, Cultured↗
PubMed1975

A selective inhibitor of the elicitation of immune-mediated reactions.

6-Chloro-17 alpha-hydroxypregna-1,4,6-triene-3,20-dione (CHP), a steroid having a progestin-type structure yet not having progestational activity, was found to exhibit moderate anti-inflammatory activity in a number of conventional tests for corticoid potency (e.g., thymolytic, granuloma, carrageenin edema). CHP was essentially equipotent, however, with cortisol in models of inflammation mediated via delayed hypersensitivity such as experimental allergic encephalomyelitis, adjuvant-induced arthritis, mouse skin graft, and mouse skin delayed hypersensitivity. In contrast to cortisol, which inhibits both 19-s and 7-s antibody formation, CHP does not diminish the number of cells producing either antibody.

Adrenal Glands↗
PubMed1971

Selective associations of hormonal steroids with aminoacyl transfer RNAs and control of protein synthesis.

The hormonal steroids progesterone, estradiol, testosterone, and 5alpha-dihydrotestosterone bind to aminoacyl-tRNA, but not to deacylated tRNA, implying that a change in conformation of tRNA occurs on aminoacylation. Binding is restricted to a few tRNA species and depends on the structure of both tRNA and steroid. There is one binding site per aminoacyl-tRNA molecule, the specificity of which appears to depend on a restricted, single-stranded loop sequence and on the tRNA conformation. By binding to an aminoacyl-tRNA, a steroid can control polypeptide synthesis in a model in vitro system by inhibiting chain elongation under conditions where aminoacyl-tRNA concentration is rate-limiting.

Acylation↗
PubMed1969

Interactions of hormonal steroids with nucelic acids. I. A specific requirement for guanine.

Under equilibrium conditions testosterone, progesterone, estradiol, and corticosterone bind to denatured but not to native DNA. Among synthetic polynucleotides, steroids bind only to guanine containing polymers:poly dG, poly G, poly UG, poly AG, and "denatured" poly dG:dC; however, they do not bind to rRNA, sRNA, TMV-RNA, poly CG, or native poly dG:dC. These data indicate a preferential affinity for guanine residues and for single-stranded regions of polynucleotides. That different functional groups of the purine are involved in the associations with different steroids is indicated by the observation that only estradiol binds to poly I. Restrictions are also imposed by structural attributes of the steroids: an alpha-substitution at C-17 reduces binding, polyhydroxylated steroids bind poorly or not at all.

Binding Sites↗