Post-treatment skin reactions reported by cancer patients differ by race, not by treatment or expectations

Cancer patients may experience skin problems while undergoing chemotherapy and radiation therapy. Frequency of skin reactions may be influenced by skin pigmentation and psychological factors. A Symptom Inventory completed by 656 cancer patients nationwide before and after chemotherapy, radiation therapy, or chemotherapy plus radiation therapy was analysed to determine if treatment type, race (Black vs White), and pretreatment expectations influenced post-treatment skin reactions. Subsequent analysis of a local Symptom Inventory completed weekly for 5 weeks by 308 patients receiving radiation therapy examined severity of reported skin reactions. Significantly more patients receiving radiation therapy had stronger expectations of skin problems (62%) than patients receiving chemotherapy (40%, P=0.001) or chemotherapy plus radiation therapy (45%, P=0.003). Overall, expectations did not correlate with patient reported post-treatment skin problems in white (r=0.014, P=0.781) or black (r=0.021, P=0.936) patients. Although no significant difference was found between black and white patients in their pretreatment expectations of skin problems (P=0.32), black patients (10 out of 18, 56%) reported more skin problems than white patients (90 out of 393, 23%, P=0.001). Similarly, the local study showed that significantly more black patients (1 out of 5, 20%) reported severe skin reactions at the treatment site than white patients (12 out of 161, 8%). A direct correlation was observed between severity of skin problems and pain at the treatment site (r=0.541, P<0.001). Total radiation exposure did not significantly correlate with the report of skin problems at the treatment site for white or black patients. Overall, black patients reported more severe post-treatment skin problems than white patients. Our results suggest that symptom management for post-treatment skin reactions in cancer patients receiving radiation treatment could differ depending on their racial background

Accumulation of the common mitochondrial DNA deletion induced by ionizing radiation

Point mutations and deletions in mitochondrial DNA (mtDNA) accumulate as a result of oxidative stress, including ionizing radiation. As a result, dysfunctional mitochondria suffer from a decline in oxidative phosphorylation and increased release of superoxides and other reactive oxygen species (ROS). Through this mechanism, mitochondria have been implicated in a host of degenerative diseases. Associated with this type of damage, and serving as a marker of total mtDNA mutations and deletions, the accumulation of a specific 4977-bp deletion, known as the common deletion (Δ-mtDNA4977), takes place. The Δ-mtDNA4977 has been reported to increase with age and during the progression of mitochondrial degeneration. The purpose of this study was to investigate whether ionizing radiation induces the formation of the common deletion in a variety of human cell lines and to determine if it is associated with cellular radiosensitivity. Cell lines used included eight normal human skin fibroblast lines, a radiosensitive non-transformed and an SV40 transformed ataxia telangiectasia (AT) homozygous fibroblast line, a Kearns Sayre Syndrome (KSS) line known to contain mitochondrial deletions, and five human tumor lines. The Δ-mtDNA4977 was assessed by polymerase chain reaction (PCR). Significant levels of Δ-mtDNA4977 accumulated 72 h after irradiation doses of 2, 5, 10 or 20 Gy in all of the normal lines with lower response in tumor cell lines, but the absolute amounts of the induced deletion were variable. There was no consistent dose-response relationship. SV40 transformed and non-transformed AT cell lines both showed significant induction of the deletion. However, the five tumor cell lines showed only a modest induction of the deletion, including the one line that was deficient in DNA damage repair. No relationship was found between sensitivity to radiation-induced deletions and sensitivity to cell killing by radiation. © 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.Alsbeih G, 2003, RADIOTHER ONCOL, V66, P341, DOI 10.1016-S0167-8140(02)00327-4; AMES BN, 1989, MUTAT RES, V214, P41, DOI 10.1016-0027-5107(89)90196-6; AMES BN, 1989, FREE RADICAL RES COM, V7, P121, DOI 10.3109-10715768909087933; ATTARDI G, 1988, ANNU REV CELL BIOL, V4, P289, DOI 10.1146-annurev.cb.04.110188.001445; Becker-Catania SG, 2000, MOL GENET METAB, V70, P122, DOI 10.1006-mgme.2000.2998; CORTOPASSI GA, 1992, P NATL ACAD SCI USA, V89, P7370, DOI 10.1073-pnas.89.16.7370; CORTOPASSI GA, 1990, NUCLEIC ACIDS RES, V18, P6927, DOI 10.1093-nar-18.23.6927; FRAGA CG, 1990, P NATL ACAD SCI USA, V87, P4533, DOI 10.1073-pnas.87.12.4533; GEARA FB, 1992, INT J RADIAT ONCOL, V24, P287; GEARA FB, 1993, INT J RADIAT ONCOL, V27, P1173; Gerhard GS, 2002, MECH AGEING DEV, V123, P155, DOI 10.1016-S0047-6374(01)00328-1; Jessie BC, 2001, EXP GERONTOL, V37, P169, DOI 10.1016-S0531-5565(01)00153-X; Khanna KK, 2001, NAT GENET, V27, P247, DOI 10.1038-85798; Kubota N, 1997, RADIAT RES, V148, P395, DOI 10.2307-3579525; Lee HC, 2001, MUTAT RES-GEN TOX EN, V493, P67, DOI 10.1016-S1383-5718(01)00160-7; LEE HC, 1994, BBA-MOL BASIS DIS, V1226, P37, DOI 10.1016-0925-4439(94)90056-6; Richard SM, 2000, CANCER RES, V60, P4231; SCHON EA, 1989, SCIENCE, V244, P346, DOI 10.1126-science.2711184; SHOFFNER JM, 1989, P NATL ACAD SCI USA, V86, P7952, DOI 10.1073-pnas.86.20.7952; SMEETS MFMA, 1993, INT J RADIAT BIOL, V63, P703, DOI 10.1080-09553009314552101; TAYLOR AMR, 1975, NATURE, V258, P427, DOI 10.1038-258427a0; Tchirkov A, 1997, HUM GENET, V101, P312, DOI 10.1007-s004390050634; WALLACE DC, 1992, ANNU REV BIOCHEM, V61, P1175, DOI 10.1146-annurev.bi.61.070192.005523; WALLACE DC, 1995, AM J HUM GENET, V57, P201; WALLACE DC, 1992, SCIENCE, V256, P628, DOI 10.1126-science.1533953; WALLACE DC, 1994, P NATL ACAD SCI USA, V91, P8739, DOI 10.1073-pnas.91.19.8739; WURM R, 1994, INT J RADIAT ONCOL, V30, P625; YEN TC, 1991, BIOCHEM BIOPH RES CO, V178, P124, DOI 10.1016-0006-291X(91)91788-E; YONEDA M, 1995, BIOCHEM BIOPH RES CO, V209, P723, DOI 10.1006-bbrc.1995.155965786

The production and composition of rat sebum is unaffected by 3 Gy gamma radiation

PURPOSE: The aim of this work was to use metabolomics to evaluate sebum as a source of biomarkers for gamma-radiation exposure in the rat, and potentially in man. Proof of concept of radiation metabolomics was previously demonstrated in both mouse and rat urine, from the radiation dose- and time-dependent excretion of a set of urinary biomarkers. MATERIALS AND METHODS: Rats were gamma-irradiated (3 Gy) or sham irradiated and groups of rats were euthanised at 1 h or 24 h post-irradiation. Sebum was collected by multiple washings of the carcasses with acetone. Nonpolar lipids were extracted, methylated, separated and quantitated using gas chromatography-mass spectrometry (GCMS). Metabolomic analysis of the GCMS data was performed using both orthogonal projection to latent structures-discriminant analysis and random forests machine learning algorithm. RESULTS: Irradiation did not alter sebum production. A total of 35 lipids were identified in rat sebum, 29 fatty acids, five fatty aldehydes, and cholesterol. Metabolomics showed that three fatty acids, palmitic, 2-hydroxypalmitic, and stearic acids were potential biomarkers. Sebaceous palmitic acid was marginally statistically significantly elevated (7.5–8.4%) at 24 h post-irradiation. CONCLUSIONS: Rat sebaceous gland appears refractory to 3 Gy gamma-irradiation. Unfortunately, collection of sebum shortly after gamma-irradiation is unlikely to form the basis of high-throughput non-invasive radiation biodosimetry in man

Manganese-reducing Pseudomonas fluorescens-group bacteria control arsenic mobility in gold mining-contaminated groundwater

Previous studies show the importance of iron- and arsenate-reducing bacteria in mobilizing arsenic in groundwater. Here the authors present experimental evidence of arsenic mobilization in connection with bacterially mediated manganese reduction in groundwater affected by mining activities. Manganese-reducing Pseudomonas species were enriched, isolated and identified by 16S rRNA gene phylogeny from groundwater containing high co-dissolved arsenic (as AsIII) and manganese. Enrichment cultures dissolved synthetic birnessite and hausmannite efficiently, but Mn reduction by isolates was reduced at the upper range of environmental levels of dissolved AsIII. Results suggest either a self-limiting release of arsenic coupled to bacterial manganese reduction, in the absence of other electron donors like sulfide, or increased arsenic resistance conferred to Mn-reducing bacteria in consortia