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41.
Iron-overload diseases frequently develop hepatocellular carcinoma. The
genotoxic mechanism whereby iron is involved in hepatocarcinogenesis might
involve an oxidative process via the intermediate production of reactive
oxygen species. This was presently investigated by examining kinetics of
formation and repair of DNA base lesions in primary rat hepatocyte cultures
supplemented with the iron chelate, ferric nitrilotriacetate Fe-NTA (10 and
100 microM). Seven DNA base oxidation products have been identified in DNA
extracts by gas chromatography- mass spectrometry, which showed a
predominance of oxidized-purines (8- oxo-guanine, xanthine, fapy-adenine,
2-oxo-adenine) above oxidized pyrimidines (5-OHMe-uracil, 5-OH-uracil,
5-OH-cytosine) in control cultures. All these DNA oxidation products
revealed a significant dose- dependent increase at 4 to 48 h after Fe-NTA
supplementation, among which fapy-adenine showed the highest increase and
5-OH-cytosine was the least prominent. Involvement of iron in this
oxidative process was established by a correlation between extent in DNA
oxidation and intracellular level of toxic low molecular weight iron. DNA
excision- repair activity was estimated by release of DNA oxidation
products in culture medium. All the seven DNA oxidation products were
detected in the medium of control cultures and showed basal repair
activity. This DNA repair activity was increased in a time- and
dose-dependent fashion with Fe-NTA. Oxidized-pyrimidines, among which was
5-OHMe-Uracil, were preferentially repaired, which explains the low levels
detected in oxidized DNA. Since oxidized bases substantially differed from
one another in terms of excision rates from cellular DNA, specific
excision- repair enzymes might be involved. Our findings, however,
demonstrate that even though DNA repair pathways were activated in
iron-loaded hepatocyte cultures, these processes were not stimulated enough
to prevent an accumulation of highly mutagenic DNA oxidative products in
genomic DNA. The resulting genotoxic effect of Fe-NTA might be relevant in
understanding the hepatocarcinogenic evolution of iron-overload diseases.
相似文献
42.
ANA JP MORAES POLLYANA MF SOARES AURA L ZAPATA ANA PN LOTITO ADRIANA ME SALLUM CLOVIS AA SILVA 《Pediatrics international》2006,48(1):48-53
Background: The purpose of the present paper was to describe the clinical manifestations and treatment of patients with panniculitis. Methods: From January 1983 to December 2002, 4294 patients were treated for pediatric rheumatological diseases at Pediatric Rheumatology Unit, University of São Paulo, Brazil. Of these, 35 children and adolescents (0.8%) presented with panniculitis: erythema nodosum (EN) or Weber–Christian disease (WCD). Clinical characteristics, laboratory exams, biopsy of the lesion, treatment and clinical course were studied. Results: Of the 35 patients, 29 presented with EN and six with WCD, one of these with cytophagic histiocytic panniculitis. Mean age at symptom onset was 85 months (6–204 months) and the mean duration of follow up was 55 months (1–144 months). All the patients presented with inflammatory subcutaneous nodules. The patients with WCD presented with systemic manifestations and cutaneous atrophy. The principal etiologies of EN were streptococcal infection (42%), undetermined (13.5%), pulmonary tuberculosis (10%), and acute rheumatic fever (10%). Biopsy of the nodules indicated septal panniculitis in 14 patients with EN and lobular panniculitis without vasculitis in the patients with WCD, one of which had cytophagic histiocytic panniculitis. There was recurrence in 11 patients (38%) with EN and in all those with WCD. Non‐steroidal anti‐inflammatory drugs were used in 15 patients with EN and corticosteroids and/or immunosuppressive drugs in the six patients with WCD. Three patients died. Conclusions: EN is the most frequent panniculitis, with a benign course and is mainly associated with infections. WCD is a severe disease, with systemic involvement, that proceeds with cutaneous atrophy and requires the use of corticosteroids and or immunosuppressive drugs. 相似文献
43.
Melanin-concentrating hormone regulates leptin synthesis and secretion in rat adipocytes 总被引:5,自引:0,他引:5
Obesity is a common problem in Western society and is associated with significant morbidity and mortality. Energy homeostasis is regulated by a complex system involving both peripheral signals such as leptin and a number of orexigenic and anorectic neuropeptides. Obesity can result from dysregulation of the peripheral and/or central signals. Melanin-concentrating hormone (MCH) is a hypothalamic peptide that is important in the regulation of feeding behavior, primarily via uncharacterized signaling pathways in the central nervous system. Leptin, expressed in adipose tissue, mediates some of its actions through several hypothalamic neuropeptides, notably agouti-related peptide, proopiomelanocortin, and neuropeptide Y. Expression of leptin is regulated by dietary status, insulin, and glucocorticoids. Furthermore, certain neuropeptides may act on adipocytes. However, the potential effect of MCH has not been investigated. We report that MCH stimulates leptin mRNA expression and leptin secretion. MCH stimulated a 2-fold increase in leptin secretion by isolated rat adipocytes after 4 h of treatment. This increase in secreted leptin was preceded by a rapid and transient increase in ob mRNA levels; MCH stimulated a 2.5-fold increase in ob mRNA within 1 h of treatment, followed by a decline to basal levels within 4 h. In addition, we demonstrate that the MCH receptor SLC-1 is expressed in adipocytes, suggesting that fat cells may be targets of MCH or an MCH-like peptide under physiological conditions. Finally, using a radioimmunoassay, MCH/MCH-like peptide was detected in rat plasma. This study establishes a novel in vitro mammalian system for examining MCH signaling pathways. 相似文献
44.
45.
Determination of malondialdehyde-induced DNA damage in human tissues using an immunoslot blot assay 总被引:3,自引:4,他引:3
Leuratti C; Singh R; Lagneau C; Farmer PB; Plastaras JP; Marnett LJ; Shuker DE 《Carcinogenesis》1998,19(11):1919-1924
Malondialdehyde (MDA) is a product of lipid peroxidation and prostaglandin
biosynthesis. It is mutagenic and carcinogenic and the major adduct formed
by reaction with DNA, a highly fluorescent pyrimidopurinone (M1-dG), has
been detected in healthy human liver and leukocyte DNA. Analytical methods
used so far for the detection of M1- dG have not been applied to a large
number of individuals or variety of samples. Often, only a few microg of
DNA from human tissues are available for analysis and a very sensitive
assay is needed in order to detect background levels of M1-dG in very small
amounts of DNA. In this paper, the development of an immunoslot blot (ISB)
assay for the measurement of MI-dG in 1 microg of DNA is described. The
limit of detection of the assay is 2.5 adducts per 10(8) bases. A series of
human samples were analysed and levels of 5.6-9.5 (n = 8) and 3.1-64.3 (n =
42) of M1-dG per 10(8) normal bases were detected in white blood cell and
gastric biopsy DNA, respectively. Results on four human samples were
compared with those obtained using an HPLC/32P-post- labelling (HPLC/PPL)
method previously developed and indicated a high correlation between M1-dG
levels measured by the two assays. The advantages of ISB over other assays
including HPLC/PPL, such as the possibility of analysing 1 microg
DNA/sample and the fact that it is less time-consuming and laborious, means
that it can be more easily used for routine analysis of a large number of
samples in biomonitoring studies.
相似文献
46.
Eimear C Morrissey Sean F Dinneen Michelle Lowry Eelco JP de Koning Marleen Kunneman 《Journal of diabetes investigation.》2022,13(8):1294
Young adults living with type 1 diabetes often struggle to achieve what clinicians consider to be optimal levels of metabolic control. Despite the impact that this can have on a young person''s future risk of complications, there are relatively few studies reporting new ways of organizing or delivering care to this cohort. In this article, we explore some of the reasons why young adult diabetes care is challenging, and describe approaches to “re‐imagining” how care might be improved. The work is informed by the ‘Making Care Fit’ collaborative and by a program of research, entitled D1 Now, involving co‐design of a complex person‐centered intervention with young adults. 相似文献
47.
Christopher Learn MD Alistair Phillips MD Joanne Chisolm BSN MSN ACNP‐BC Sharon Hill MSN ACNP‐BC John Cheatham MD Peter Winch MD MBA Mark Galantowicz MD Ralf Holzer MD 《Congenital heart disease》2012,7(2):111-121
Introduction. Pulmonary atresia with ventricular septal defect (VSD) continues to be associated with significant morbidity and mortality, with significant institutional variation in therapeutic strategies. This study reports a single center experience utilizing an intensive transcatheter approach to promote pulmonary vascular growth. Methods. A retrospective analysis of 20 patients undergoing surgical and transcatheter treatment for pulmonary atresia with VSD between 2002 and 2010. Results. The median age at initial surgical palliation was 6.3 months (8 days to 2.5 years). Eleven patients (group 1) underwent initial surgical palliation without VSD closure and nine patients (group 2) underwent an initial complete repair with fenestrated or complete VSD closure. Group 1 had a smaller Nakata index (54 mm2/m2 vs. 134 mm2/m2, P= .04) and a smaller absolute native pulmonary artery diameter (2.7 mm vs. 4.5 mm, P= .01) than group 2. Intraoperative angiography was performed in 10 cases to evaluate if early transcatheter intervention was warranted. The median follow‐up during the study period was 2.3 years (1.6 months to 8.3 years). Of the 16 patients who survived the initial early postoperative period, 15 patients (94%) went on to receive surgical (n = 11) and/or interventional (n = 25) catheterization procedures. There was improvement in the mean Nakata index from the initial presurgical evaluation to the most recent catheterization data (38.4 mm2/m2 vs. 169.7 mm2/m2, P≤ .05). To date, two of 11 (18%) patients in group 1 ultimately underwent surgical VSD closure. Overall mortality was six of 20 (30%) with four deaths in group 1 and two deaths in group 2. There were no procedural deaths. Conclusions. Combining surgical unifocalization procedures with subsequent early and intensive catheter‐based pulmonary artery rehabilitation may improve vascular growth, ultimately rendering many patients suitable for fenestrated VSD closure. Risk stratification, including intraoperative exit angiography, is essential to determine the need for early transcatheter interventions. 相似文献
48.
49.