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Mitochondria,nitric oxide,and cardiovascular dysfunction 总被引:6,自引:0,他引:6
Ramachandran A Levonen AL Brookes PS Ceaser E Shiva S Barone MC Darley-Usmar V 《Free radical biology & medicine》2002,33(11):1465-1474
Cardiovascular diseases encompass a wide spectrum of abnormalities with diverse etiologies. The molecular mechanisms underlying these disorders include a variety of responses such as changes in nitric oxide- (NO) dependent cell signaling and increased apoptosis. An interesting aspect that has received little or no attention is the role mitochondria may play in the vascular changes that occur in both atherosclerosis and hypertension. With the changing perspective of the organelle from simply a role in metabolism to a contributor to signal transduction pathways, the role of mitochondria in cells with relatively low energy demands such as the endothelium has become important to understand. In this context, the definition of the NO-cytochrome c oxidase signaling pathway and the influence this has on cytochrome c release is particularly important in understanding apoptotic mechanisms involving the mitochondrion. This review examines the role of compromised mitochondrial function in a variety of vascular pathologies and the modulation of these effects by NO. The interaction of NO with the various mitochondrial respiratory complexes and the role NO plays in modulating mitochondrial-mediated apoptosis in these systems will be discussed. 相似文献
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Li C Kotha S Huang CH Mason J Yakimicki D Hawkins M 《Journal of biomechanical engineering》2003,125(3):315-322
A finite element technique was developed to investigate the thermal behavior of bone cement in joint replacement procedures. Thermal tests were designed and performed to provide the parameters in a kinetic model of bone cement exothermic polymerization. The kinetic model was then coupled with an energy balance equation using a finite element formulation to predict the temperature history and polymerization development in the bone-cement-prosthesis system. Based on the temperature history, the possibility of the thermal bone necrosis was then evaluated. As a demonstration, the effect of cement mantle thickness on the thermal behavior of the system was investigated. The temperature profiles in the bone-cement-prosthesis system have shown that the thicker the cement, the higher the peak temperature in the bone. In the 7 mm thick cement case, a peak temperature of over 55 degrees C was predicted. These high temperatures occurred in a small region near the bone/cement interface. No damage was predicted in the 3 mm and 5 mm cement mantle thickness cases. Although thermal damage was predicted in the bone for the 7 mm mantle thickness case, the amount of thermal necrosis predicted was minimal. If more cement is used in the surgical procedure, more heat will be generated and the potential for thermal bone damage may rise. The systems should be carefully selected to reduce thermal tissue damage when more cement is used. The methodology developed in this paper provides a numerical tool for the quantitative simulation of the thermal behavior of bone-cement-prosthesis designs. 相似文献
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Mohagheghzadeh Abdolali Hemmati Shiva Mehregan Iraj Alfermann A. Wilhelm 《Phytochemistry Reviews》2003,2(3):363-369
Aryltetralin lignans (podophyllotoxin type) are the main lignan constituents of species belonging to Linum section Syllinum (Linaceae). Linum persicum, a perennial plant native to Iran closely related to L. album, has not yet been studied. To evaluate the lignan profile, fresh plants of L. persicumwere collected and divided into different parts and analyzed by HPLC. The main aryltetralin lignans found inL. persicumplant parts, callus and cell cultures were podophyllotoxin (PTOX), 6-methoxypodophyllotoxin (MPTOX) and - and -peltatin. Furthermore, the systematic relationship between L. persicum and other Linum species are discussed in the light of morphological and phytochemical aspects.
Abbreviations: MPTOX – 6-methoxypodophyllotoxin; PTOX – podophyllotoxin; DOP – deoxypodophyllotoxin. 相似文献
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Keshava Nagalakshmi Zhou Gu Spruill Michelle Ensell Mang Ong Tong-man 《Molecular and cellular biochemistry》2001,222(1-2):69-76
Occupational exposure to beryllium (Be) and Be compounds occurs in a wide range of industrial processes. A large number of workers are potentially exposed to this metal during manufacturing and processing, so there is a concern regarding the potential carcinogenic hazard of Be. Studies were performed to determine the carcinogenic potential of beryllium sulfate (BeSO4) in cultured mammalian cells. BALB/c3T3 cells were treated with varying concentrations of BeSO4 for 72 h and the transformation frequency was determined after 4 weeks of culturing. Concentrations from 50–200 g BeSO4/ml, caused a concentrationdependent increase (9–41 fold) in transformation frequency. Nontransformed BALB/c3T3 cells and cells from transformed foci induced by BeSO4 were injected into both axillary regions of nude mice. All ten Beinduced transformed cell lines injected into nude mice produced fibrosarcomas within 50 days after cell injection. No tumors were found in nude mice receiving nontransformed BALB/c3T3 cells 90 days postinjection. Gene amplification was investigated in Kras, cmyc, cfos, cjun, csis, erbB2 and p53 using differential PCR while random amplified polymorphic DNA fingerprinting was employed to detect genomic instability. Gene amplification was found in Kras and cjun, however no change in gene expression or protein level was observed in any of the genes by Western blotting. Five of the 10 transformed cell lines showed genetic instability using different random primers. In conclusion, these results indicate that BeSO4 is capable of inducing morphological cell transformation in mammalian cells and that transformed cells induced by BeSO4 are potentially tumorigenic. Also, cell transformation induced by BeSO4 may be attributed, in part, to the gene amplification of Kras and cjun and some BeSO4induced transformed cells possess neoplastic potential resulting from genomic instability. 相似文献
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Analysis of K-ras and p53 mutations in mesotheliomas from humans and rats exposed to asbestos 总被引:3,自引:0,他引:3
Malignant mesothelioma is known to be associated with asbestos exposure. However, the mechanism of mesothelial carcinogenesis in relation to the activation of proto-oncogenes or inactivation of tumor suppressor genes remains unclear. In this study, the PCR-Primer Introduced Restriction Site (PCR-PIRS) assay was employed to examine mutations in the K-ras proto-oncogene in mesothelioma tissues from workers exposed to asbestos and from rats treated with asbestos. Mutations in exons 5-8 of the p53 tumor suppressor gene were determined by direct DNA sequence analysis. Results of the PCR-PIRS analysis revealed no mutations in codons 12, 13 or 61 of the K-ras gene in any of the 17 human or 22 rat mesothelioma tissue samples. These results were confirmed by direct DNA sequence analysis. No mutations were found in exons 5-8 of the p53 gene in any of the mesothelioma tissue samples analyzed. These results and the results reported by others indicate that the K-ras proto-oncogene and p53 tumor suppressor gene may not play a critical role in the induction of mesothelioma by asbestos either in humans or in rats. 相似文献
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Hernando Gomez Benjamin Kautza Daniel Escobar Ibrahim Nassour Jason Luciano Ana Maria Botero Lisa Gordon Silvia Martinez Andre Holder Olufunmilayo Ogundele Patricia Loughran Matthew R. Rosengart Michael Pinsky Sruti Shiva Brian S. Zuckerbraun 《PloS one》2015,10(9)