RESUMO
BACKGROUND: We aimed to demonstrate the effects of tumor treating fields (TTFields) in head and neck squamous cell carcinoma (HNSCC) cells when combined with radiotherapy (RT) and chemotherapy. METHODS: Two human HNSCC cell lines (Cal27, FaDu) received five different treatments: TTFields, RT +/- TTFields and RT + simultaneous cisplatin +/- TTFields. Effects were quantified using clonogenic assays and flow cytometric analyses of DAPI, caspase-3 activation and γH2AX foci. RESULTS: Treatment with RT + TTFields decreased the clonogenic survival as strong as treatment with RT + simultaneous cisplatin. The triple combination of RT + simultaneous cisplatin + TTFields even further decreased the clonogenic survival. Accordingly, combination of TTFields with RT or RT + simultaneous cisplatin increased cellular apoptosis and DNA double-strand breaks. CONCLUSION: TTFields therapy seems a promising combination partner in the multimodal treatment of locally advanced HNSCC. It could be used to intensify chemoradiotherapy or as alternative to chemotherapy.
Assuntos
Cisplatino , Neoplasias de Cabeça e Pescoço , Humanos , Carcinoma de Células Escamosas de Cabeça e Pescoço/terapia , Neoplasias de Cabeça e Pescoço/terapia , Terapia Combinada , QuimiorradioterapiaRESUMO
The influence of high-linear energy transfer (LET) particle radiation on the functionalities of mesenchymal stromal cells (MSCs) is largely unknown. Here, we analyzed the effects of proton (1H), helium (4He), carbon (12C) and oxygen (16O) ions on human bone marrow-MSCs. Cell cycle distribution and apoptosis induction were examined by flow cytometry, and DNA damage was quantified using γH2AX immunofluorescence and Western blots. Relative biological effectiveness values of MSCs amounted to 1.0-1.1 for 1H, 1.7-2.3 for 4He, 2.9-3.4 for 12C and 2.6-3.3 for 16O. Particle radiation did not alter the MSCs' characteristic surface marker pattern, and MSCs maintained their multi-lineage differentiation capabilities. Apoptosis rates ranged low for all radiation modalities. At 24 h after irradiation, particle radiation-induced ATM and CHK2 phosphorylation as well as γH2AX foci numbers returned to baseline levels. The resistance of human MSCs to high-LET irradiation suggests that MSCs remain functional after exposure to moderate doses of particle radiation as seen in normal tissues after particle radiotherapy or during manned space flights. In the future, in vivo models focusing on long-term consequences of particle irradiation on the bone marrow niche and MSCs are needed.
Assuntos
Proteínas Mutadas de Ataxia Telangiectasia/genética , Quinase do Ponto de Checagem 2/genética , Histonas/genética , Células-Tronco Mesenquimais/efeitos da radiação , Células-Tronco/efeitos da radiação , Medicina Aeroespacial , Apoptose/genética , Apoptose/efeitos da radiação , Células da Medula Óssea/metabolismo , Células da Medula Óssea/patologia , Células da Medula Óssea/efeitos da radiação , Carbono/efeitos adversos , Ciclo Celular/genética , Ciclo Celular/efeitos da radiação , Linhagem da Célula/genética , Linhagem da Célula/efeitos da radiação , Citometria de Fluxo , Regulação da Expressão Gênica/efeitos da radiação , Hélio/efeitos adversos , Humanos , Células-Tronco Mesenquimais/metabolismo , Oxigênio/efeitos adversos , Prótons/efeitos adversos , Voo Espacial , Células-Tronco/metabolismoRESUMO
Albeit being an effective therapy for various cutaneous conditions, UV-B irradiation can cause severe skin damage. While multipotent mesenchymal stem cells (MSCs) may aid the regeneration of UV-B-induced skin injuries, the influence of UV-B irradiation on MSCs remains widely unknown. Here, we show that human MSCs are relatively resistant to UV-B irradiation compared to dermal fibroblasts. MSCs exhibited higher clonogenic survival, proliferative activity and viability than dermal fibroblasts after exposure to UV-B irradiation. Cellular adhesion, morphology and expression of characteristic surface marker patterns remained largely unaffected in UV-irradiated MSCs. The differentiation ability along the adipogenic, osteogenic and chondrogenic lineages was preserved after UV-B treatment. However, UV-B radiation resulted in a reduced ability of MSCs and dermal fibroblasts to migrate. MSCs exhibited low apoptosis rates after UV-B irradiation and repaired UV-B-induced cyclobutane pyrimidine dimers more efficiently than dermal fibroblasts. UV-B irradiation led to prolonged p53 protein stability and increased p21 protein expression resulting in a prolonged G2 arrest and senescence induction in MSCs. The observed resistance may contribute to the ability of these multipotent cells to aid the regeneration of UV-B-induced skin injuries.
Assuntos
Células-Tronco Mesenquimais/efeitos da radiação , Raios Ultravioleta , Diferenciação Celular/efeitos da radiação , Proliferação de Células/efeitos da radiação , Sobrevivência Celular/efeitos da radiação , Humanos , Pele/lesões , Pele/patologia , CicatrizaçãoRESUMO
The presented method or slightly modified versions have been devised to study specific treatment responses and side effects of various anti-cancer treatments as used in clinical oncology. It enables a quantitative and longitudinal analysis of the DNA damage response after genotoxic stress, as induced by radiotherapy and a multitude of anti-cancer drugs. The method covers all stages of the DNA damage response, providing endpoints for induction and repair of DNA double-strand breaks (DSBs), cell cycle arrest and cell death by apoptosis in case of repair failure. Combining these measurements provides information about cell cycle-dependent treatment effects and thus allows an in-depth study of the interplay between cellular proliferation and coping mechanisms against DNA damage. As the effect of many cancer therapeutics including chemotherapeutic agents and ionizing radiation is limited to or strongly varies according to specific cell cycle phases, correlative analyses rely on a robust and feasible method to assess the treatment effects on the DNA in a cell cycle-specific manner. This is not possible with single-endpoint assays and an important advantage of the presented method. The method is not restricted to any particular cell line and has been thoroughly tested in a multitude of tumor and normal tissue cell lines. It can be widely applied as a comprehensive genotoxicity assay in many fields of oncology besides radio-oncology, including environmental risk factor assessment, drug screening and evaluation of genetic instability in tumor cells.
Assuntos
Apoptose/efeitos dos fármacos , Dano ao DNA , Citometria de Fluxo/métodos , Radioterapia com Íons Pesados , Histonas/metabolismo , Fótons , Apoptose/efeitos da radiação , Ciclo Celular/fisiologia , Ciclo Celular/efeitos da radiação , Pontos de Checagem do Ciclo Celular , Divisão Celular , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Quebras de DNA de Cadeia Dupla , Reparo do DNA , Glioblastoma , Humanos , Fosforilação , Radiação IonizanteRESUMO
BACKGROUND: Mesenchymal stem cells (MSCs) participate in the regeneration of tissue lesions induced by antimetabolite chemotherapy; however, the influence of this class of anti-cancer compounds on the stem cells remains largely unknown. METHODS: The survival of MSCs after exposure to 5-fluorouracil (5-FU) and gemcitabine was measured by viability and clonogenic assays. MSC morphology, surface marker expression, adhesion potential, cellular velocity and differentiation potential were determined after antimetabolite treatment. Cell cycle distribution and apoptosis were assessed using flow cytometry, and senescence induction was evaluated by beta-galactosidase staining. Gene expression arrays were used to analyze the expression of enzymes involved in DNA metabolism and multidrug resistance. RESULTS: Here, we show that human primary bone marrow MSCs are relatively resistant to treatment with the widely used antimetabolite drugs 5-FU and gemcitabine. The stem cells were able to largely retain their functional abilities and defining stem cell traits after antimetabolite exposure. MSCs surface markers were found stably expressed, and the characteristic multi-lineage differentiation potential was maintained irrespective of 5-FU or gemcitabine treatment. High expression levels of enzymes involved in DNA metabolism and multidrug resistance transporters may contribute to the resistance to antimetabolite chemotherapy. DISCUSSION: The observed resistance and functional integrity may form the basis for further investigations of MSCs as a potential therapy for antimetabolite-induced tissue damage.
Assuntos
Antimetabólitos/farmacologia , Diferenciação Celular/efeitos dos fármacos , Adipogenia/efeitos dos fármacos , Células da Medula Óssea/citologia , Adesão Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Desoxicitidina/análogos & derivados , Desoxicitidina/farmacologia , Fibroblastos/citologia , Fibroblastos/metabolismo , Fluoruracila/farmacologia , Humanos , Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/metabolismo , Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética , Proteínas Associadas à Resistência a Múltiplos Medicamentos/metabolismo , GencitabinaRESUMO
Chemotherapy constitutes one of the key treatment modalities for solid and hematological malignancies. Albeit being an effective treatment, chemotherapy application is often limited by its damage to healthy tissues, and curative treatment options for chemotherapy-related side effects are largely missing. As mesenchymal stromal cells (MSCs) are known to exhibit regenerative capacity mainly by supporting a beneficial microenvironment for tissue repair, MSC-based therapies may attenuate chemotherapy-induced tissue injuries. An increasing number of animal studies shows favorable effects of MSC-based treatments; however, clinical trials for MSC therapies in the context of chemotherapy-related side effects are rare. In this concise review, we summarize the current knowledge of the effects of MSCs on chemotherapy-induced tissue toxicities. Both preclinical and early clinical trials investigating MSC-based treatments for chemotherapy-related side reactions are presented, and mechanistic explanations about the regenerative effects of MSCs in the context of chemotherapy-induced tissue damage are discussed. Furthermore, challenges of MSC-based treatments are outlined that need closer investigations before these multipotent cells can be safely applied to cancer patients. As any pro-tumorigenicity of MSCs needs to be ruled out prior to clinical utilization of these cells for cancer patients, the pro- and anti-tumorigenic activities of MSCs are discussed in detail.
Assuntos
Antineoplásicos/efeitos adversos , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/metabolismo , Animais , Antineoplásicos/uso terapêutico , Ensaios Clínicos como Assunto , Humanos , Células-Tronco Mesenquimais/patologiaRESUMO
BACKGROUND AND PURPOSE: Carbon ion radiotherapy is a promising therapeutic option for glioblastoma patients due to its high physical dose conformity and greater biological effectiveness than photons. However, the biological effects of carbon ion radiation are still incompletely understood. Here, we systematically compared the biological effects of clinically used carbon ion radiation to photon radiation with emphasis on DNA repair. MATERIALS AND METHODS: Two human glioblastoma cell lines (U87 and LN229) were irradiated with carbon ions or photons and DNA damage response was systematically analyzed, including clonogenic survival, induction and repair of DNA double-strand breaks (DSBs), cell cycle arrest and apoptosis or autophagy. γH2AX foci were analyzed by flow cytometry, conventional light microscopy and 3D superresolution microscopy. RESULTS: DSBs were repaired delayed and with slower kinetics after carbon ions versus photons. Carbon ions caused stronger and longer-lasting cell cycle delays, predominantly in G2 phase, and a higher rate of apoptosis. Compared to photons, the effectiveness of carbon ions was less cell cycle-dependent. Homologous recombination (HR) appeared to be more important for DSB repair after carbon ions versus photons in phosphatase and tensin homolog (PTEN)-deficient U87 cells, as opposed to PTEN-proficient LN229 cells. CONCLUSION: Carbon ions induced more severe DSB damage than photons, which was repaired less efficiently in both cell lines. Thus, carbon ion radiotherapy may help to overcome resistance mechanisms of glioblastoma associated with DNA repair for example in combination with repair pathway-specific drugs in the context of personalized radiotherapy.
Assuntos
Neoplasias Encefálicas/radioterapia , Quebras de DNA de Cadeia Dupla , Glioblastoma/radioterapia , Radioterapia com Íons Pesados/métodos , Fótons/uso terapêutico , Apoptose/efeitos da radiação , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Pontos de Checagem do Ciclo Celular/efeitos da radiação , Linhagem Celular Tumoral , Reparo do DNA/efeitos da radiação , DNA de Neoplasias/genética , DNA de Neoplasias/efeitos da radiação , Glioblastoma/genética , Glioblastoma/patologia , Recombinação Homóloga/efeitos da radiação , HumanosRESUMO
Chemotherapeutic agents are part of the standard treatment algorithms for many malignancies; however, their application and dosage are limited by their toxic effects to normal tissues. Chemotherapy-induced toxicities can be long-lasting and may be incompletely reversible; therefore, causative therapies for chemotherapy-dependent side effects are needed, especially considering the increasing survival rates of treated cancer patients. Mesenchymal stem cells (MSCs) have been shown to exhibit regenerative abilities for various forms of tissue damage. Preclinical data suggest that MSCs may also help to alleviate tissue lesions caused by chemotherapeutic agents, mainly by establishing a protective microenvironment for functional cells. Due to the systemic administration of most anticancer agents, the effects of these drugs on the MSCs themselves are of crucial importance to use stem cell-based approaches for the treatment of chemotherapy-induced tissue toxicities. Here, we present a concise review of the published data regarding the influence of various classes of chemotherapeutic agents on the survival, stem cell characteristics and physiological functions of MSCs. Molecular mechanisms underlying the effects are outlined, and resulting challenges of MSC-based treatments for chemotherapy-induced tissue injuries are discussed.
Assuntos
Antineoplásicos/efeitos adversos , Células-Tronco Mesenquimais/citologia , Algoritmos , Animais , Antineoplásicos/farmacologia , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/prevenção & controle , Humanos , Transplante de Células-Tronco Mesenquimais/métodos , Células-Tronco Mesenquimais/efeitos dos fármacosRESUMO
BACKGROUND: Fibrosis is a delayed side effect of radiation therapy (RT). Connective tissue growth factor (CTGF) promotes the development of fibrosis in multiple settings, including pulmonary radiation injury. METHODS: To better understand the cellular interactions involved in RT-induced lung injury and the role of CTGF in these responses, microarray expression profiling was performed on lungs of irradiated and non-irradiated mice, including mice treated with the anti-CTGF antibody pamrevlumab (FG-3019). Between group comparisons (Welch's t-tests) and principal components analyses were performed in Genespring. RESULTS: At the mRNA level, the ability of pamrevlumab to prolong survival and ameliorate RT-induced radiologic, histologic and functional lung deficits was correlated with the reversal of a clear enrichment in mast cell, macrophage, dendritic cell and mesenchymal gene signatures. Cytokine, growth factor and matrix remodeling genes that are likely to contribute to RT pneumonitis and fibrosis were elevated by RT and attenuated by pamrevlumab, and likely contribute to the cross-talk between enriched cell-types in injured lung. CONCLUSIONS: CTGF inhibition had a normalizing effect on select cell-types, including immune cells not typically regarded as being regulated by CTGF. These results suggest that interactions between RT-recruited cell-types are critical to maintaining the injured state; that CTGF plays a key role in this process; and that pamrevlumab can ameliorate RT-induced lung injury in mice and may provide therapeutic benefit in other immune and fibrotic disorders.
Assuntos
Anticorpos Monoclonais/farmacologia , Fator de Crescimento do Tecido Conjuntivo/metabolismo , Pulmão/metabolismo , Pulmão/efeitos da radiação , Fibrose Pulmonar/metabolismo , Lesões Experimentais por Radiação/metabolismo , Animais , Anticorpos Monoclonais/uso terapêutico , Anticorpos Monoclonais Humanizados , Fator de Crescimento do Tecido Conjuntivo/antagonistas & inibidores , Feminino , Expressão Gênica , Pulmão/efeitos dos fármacos , Mastócitos/efeitos dos fármacos , Mastócitos/metabolismo , Mastócitos/efeitos da radiação , Camundongos , Camundongos Endogâmicos C57BL , Fibrose Pulmonar/tratamento farmacológico , Fibrose Pulmonar/etiologia , Lesões Experimentais por Radiação/tratamento farmacológicoRESUMO
Mesenchymal stem cells (MSCs) are an integral part of the bone marrow niche and aid in the protection, regeneration and proliferation of hematopoietic stem cells after exposure to myelotoxic taxane anti-cancer agents, but the influence of taxane compounds on MSCs themselves remains incompletely understood. Here, we show that bone marrow-derived MSCs are highly sensitive even to low concentrations of the prototypical taxane compound paclitaxel. While MSCs remained metabolically viable, they were strongly impaired regarding both their proliferation and their functional capabilities after exposure to paclitaxel. Paclitaxel treatment resulted in reduced cell migration, delays in cellular adhesion and significant dose-dependent inhibition of the stem cells' characteristic multi-lineage differentiation potential. Cellular morphology and expression of the defining surface markers remained largely unaltered. Paclitaxel only marginally increased apoptosis in MSCs, but strongly induced premature senescence in these stem cells, thereby explaining the preservation of the metabolic activity of functionally inactivated MSCs. The reported sensitivity of MSC function to paclitaxel treatment may help to explain the severe bone marrow toxicities commonly caused by taxane-based anti-cancer treatments.
Assuntos
Antineoplásicos/farmacologia , Células da Medula Óssea/efeitos dos fármacos , Células-Tronco Mesenquimais/efeitos dos fármacos , Paclitaxel/farmacologia , Apoptose , Células da Medula Óssea/citologia , Diferenciação Celular , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Células Cultivadas , Senescência Celular , Humanos , Células-Tronco Mesenquimais/citologiaRESUMO
Carbon ion radiation is a promising new form of radiotherapy for cancer, but the central question about the biologic effects of charged particle radiation is yet incompletely understood. Key to this question is the understanding of the interaction of ions with DNA in the cell's nucleus. Induction and repair of DNA lesions including double-strand breaks (DSBs) are decisive for the cell. Several DSB repair markers have been used to investigate these processes microscopically, but the limited resolution of conventional microscopy is insufficient to provide structural insights. We have applied superresolution microscopy to overcome these limitations and analyze the fine structure of DSB repair foci. We found that the conventionally detected foci of the widely used DSB marker γH2AX (Ø 700-1000 nm) were composed of elongated subfoci with a size of â¼100 nm consisting of even smaller subfocus elements (Ø 40-60 nm). The structural organization of the subfoci suggests that they could represent the local chromatin structure of elementary DSB repair units at the DSB damage sites. Subfocus clusters may indicate induction of densely spaced DSBs, which are thought to be associated with the high biologic effectiveness of carbon ions. Superresolution microscopy might emerge as a powerful tool to improve our knowledge of interactions of ionizing radiation with cells.-Lopez Perez, R., Best, G., Nicolay, N. H., Greubel, C., Rossberger, S., Reindl, J., Dollinger, G., Weber, K.-J., Cremer, C., Huber, P. E. Superresolution light microscopy shows nanostructure of carbon ion radiation-induced DNA double-strand break repair foci.
Assuntos
Quebras de DNA de Cadeia Dupla , Reparo do DNA/fisiologia , Radioterapia com Íons Pesados , Microscopia/métodos , Linhagem Celular Tumoral , Regulação da Expressão Gênica , Histonas/genética , Histonas/metabolismo , HumanosRESUMO
Mesenchymal stem cells (MSCs) aid the regeneration of tissues damaged by treatment with cisplatin. However, the effects of this cytotoxic drug on the stem cells have been largely unknown. Here we demonstrate that human bone marrow-derived MSCs are relatively resistant to cisplatin treatment and show resistance levels comparable to these of differentiated fibroblasts. Cisplatin did not affect cellular morphology, adhesion or induction of apoptosis in MSCs. The potential for differentiation was preserved after exposure to cisplatin, and established MSC surface markers were observed to be stably expressed irrespective of cisplatin treatment. Cytoskeletal rearrangements and high expression levels of individual heat shock proteins were detected in MSCs and may be partly responsible for the observed cisplatin resistance. The cisplatin-resistant phenotype of human MSCs supports the concept of further investigating these stem cells as a potential treatment option for cisplatin-induced tissue damage.
Assuntos
Cisplatino/administração & dosagem , Resistência a Medicamentos/genética , Células-Tronco Mesenquimais/efeitos dos fármacos , Regeneração/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Células da Medula Óssea/citologia , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/genética , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , Células Cultivadas , Fibroblastos/efeitos dos fármacos , Humanos , Células-Tronco Mesenquimais/citologia , FenótipoRESUMO
Mesenchymal stem cells (MSCs) comprise a heterogeneous population of multipotent stromal cells and can be isolated from various tissues and organs. Due to their regenerative potential, they have been subject to intense research efforts, and they may provide an efficient means for treating radiation-induced tissue damage. MSCs are relatively resistant to ionizing radiation and retain their stem cell characteristics even after high radiation doses. The underlying mechanisms for the observed MSC radioresistance have been extensively studied and may involve efficient DNA damage recognition, double strand break repair and evasion of apoptosis. Here, we present a concise review of the published scientific data on the radiobiological features of MSCs. The involvement of different DNA damage recognition and repair pathways in the creation of a radioresistant MSC phenotype is outlined, and the roles of apoptosis, senescence and autophagy regarding the reported radioresistance are summarized. Finally, potential influences of the radioresistant MSCs for the clinic are discussed with respect to the repair and radioprotection of irradiated tissues.
Assuntos
Regeneração Tecidual Guiada/métodos , Células-Tronco Mesenquimais/efeitos da radiação , Animais , Diferenciação Celular/efeitos da radiação , Dano ao DNA , Reparo do DNA , Humanos , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/citologia , Tolerância a RadiaçãoRESUMO
Mesenchymal stem cells (MSCs) have been isolated from various organ sites including bone marrow, skin, vascular and adipose tissues and form a heterogeneous population of multipotent stromal cells. They have been shown to exhibit a relative radiation resistance and retain their stem cell properties even after high doses of ionizing radiation. The regenerative potential of MSCs has been widely studied in the context of ischemic or mechanical forms of tissue damage, and these stem cells may also constitute a powerful means of treating tissue lesions caused by ionizing radiation, either after accidental exposure to radioactivity or as a side effect of clinical radiotherapy. Animal studies and early clinical experiences suggest a role for MSCs in the regeneration of these tissue lesions both by differentiating into functional parenchymal cells and by creating a nurturing microenvironment for other cells. Here, we review the published data on the regenerative properties of MSCs in the context of organ-specific radiation damage. Potential mechanisms and clinical applications are outlined, and problems and challenges of MSC-based treatments for radiation injuries in the clinic are summarized.
Assuntos
Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/fisiologia , Lesões por Radiação/fisiopatologia , Lesões por Radiação/terapia , Regeneração/fisiologia , Medula Óssea/metabolismo , Osso e Ossos/fisiologia , Osso e Ossos/efeitos da radiação , Proliferação de Células/fisiologia , Humanos , Intestinos/fisiologia , Intestinos/efeitos da radiação , Fígado/fisiologia , Fígado/efeitos da radiação , Pulmão/fisiologia , Pulmão/efeitos da radiação , Lesões por Radiação/prevenção & controle , Glândulas Salivares/fisiologia , Glândulas Salivares/efeitos da radiação , Fenômenos Fisiológicos da Pele/efeitos da radiaçãoRESUMO
Mesenchymal stem cells (MSCs) participate in regeneration of tissues damaged by ionizing radiation. However, radiation can damage MSCs themselves. Here we show that cellular morphology, adhesion and migration abilities were not measurably altered by photon or carbon ion irradiation. The potential for differentiation was unaffected by either form of radiation, and established MSC surface markers were found to be stably expressed irrespective of radiation treatment. MSCs were able to efficiently repair DNA double strand breaks induced by both high-dose photon and carbon ion radiation. We have shown for the first time that MSCs are relatively resistant to therapeutic carbon ion radiotherapy. Additionally, this form of radiation did not markedly alter the defining stem cell properties or the expression of established surface markers in MSCs.
Assuntos
Células-Tronco Mesenquimais/metabolismo , Células-Tronco Mesenquimais/efeitos da radiação , Radiação Ionizante , Transcriptoma/efeitos da radiação , Western Blotting , Adesão Celular/efeitos da radiação , Diferenciação Celular/efeitos da radiação , Movimento Celular/efeitos da radiação , Sobrevivência Celular/efeitos da radiação , Células Cultivadas , Quebras de DNA de Cadeia Dupla/efeitos da radiação , Reparo do DNA/efeitos da radiação , Relação Dose-Resposta à Radiação , Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos da radiação , Humanos , Células-Tronco Mesenquimais/citologia , Análise de Sequência com Séries de Oligonucleotídeos , Imagem com Lapso de TempoRESUMO
Sedimentation on reef communities at Bahías de Huatulco, Oaxaca, Mexico. Although coral reef sedimentation is important because it modifies processes like symbioses, reproduction, recruitment and coral growth, Mexican Pacific studies are lacking. On this regard, spatio-temporal variations in sedimentation rate were investigated in six coral reef communities from Oaxaca. During February 2006-January 2007 (excluding April, July and August) two sediment structures, with four sediment traps each, were randomly installed. Sediment traps were replaced with a mean periodicity of 38 days, and the sediments were washed, filtered, dried and weighted in order to calculate sedimentation rate. Sedimentation rate was heterogeneous among localities 7.06, P < 0.01). It was high at Isla Montosa (653.31 kg m-2 year-1) and Isla Cacaluta (450.09 kg m-2 (F5,36 = year-1), intermediate at San Agustín, Jicaral-Chachacual and Dos Hermanas (155.18-92.53 kg m-2 year-1) and low at La Entrega (14.33 kg m-2 year-1). Sedimentation rate was homogeneous through time (F7,34 = 0.85, P > 0.5); nonetheless, during the dry season (November-March) sedimentation rate in the area oscillated between 6.8-73.5 mg cm-2 day-1, whereas during the rainy season (May-October) the values were 141-1088 % higher (74.5-147.6 mg cm-2 day-1, Mann-Whitney U = 137, n = 42, P = 0.03). There was a significant relationship between sedimentation rate and pluvial precipitation (Spearman R = 0.83, n = 8, P = 0.009), suggesting that the amount of sediment reaching coral communities is closely tied to regional precipitation. Sedimentation rates recorded at Isla Montosa (366.64 mg cm-2 day-1) and Isla Cacaluta (366.03 mg cm-2 day-1) during the rainy season can be considered lethal-sublethal considering sediment tolerance and rejection efficiency of stony corals. The absence of coral mortality during the rainy season may result from: a) high efficiency of active sediment removal, b) increased physiological tolerance to sediments, and c) a high degree of passive sediment removal via turbulence. Nonetheless, the combined effect of natural and anthropogenic induced sedimentation may cause a shift in coral community structure and eventually a loss of the reef areas in Bahías de Huatulco. Rev. Biol. Trop. 56 (3): 11791187. Epub 2008 September 30.
Aún cuando la sedimentación en arrecifes es importante pues sus efectos alteran procesos como la simbiosis, reproducción, reclutamiento y crecimiento, se carece de estudios en el Pacífico mexicano. Debido a lo anterior, se evaluó la tasa de sedimentación y su variación espacio-temporal en seis comunidades coralinas de Oaxaca. Durante febrero 2006- enero 2007 (exceptuando abril, julio y agosto), instalamos al azar dos estructuras con cuatro recolectores de sedimento cada una. Los recolectores fueron reemplazados aproximadamente cada 38 días y los sedimentos fueron enjuagados, filtrados, secados y pesados. La tasa de sedimentación fue heterogénea entre localidades 7.06, P < 0.01); fue alta en Isla Montosa (653.31 (F5,36 = kg m-2 año-1) e Isla Cacaluta (450.09 kg m-2 año-1), inter-media en San Agustín, Jicaral-Chachacual y Dos Hermanas (155.18-92.53 kg m-2 año-1) y baja en La Entrega (14.33 kg m-2 año-1). La tasa de sedimentación no varió a lo largo del año (F7,34 = 0.85, P > 0.5); no obstante, durante la temporada de secas (noviembre-marzo) la tasa de sedimentación en la zona osciló entre 6.8-73.5 mg cm-2 día-1, mientras que durante lluvias (mayo-octubre) osciló entre 74.5-147.6 mg cm-2 día-1, es decir, durante la temporada de lluvias la tasa de sedimentación fue 141-1088 % mayor que durante secas (Mann-Whitney U = 137, n = 42, P = 0.03). La relación entre la cantidad de sedimento y la precipitación pluvial fue significativa (Spearman R = 0.83, n = 8, P = 0.009), sugiriendo que el aporte de sedimento está relacionado con la escorrentía regional. La tasa de sedimentación registrada en Isla Montosa (366.64 mg cm-2 día-1) e Isla Cacaluta (366.03 mg cm-2 día-1) durante la temporada de lluvias, puede ser considerada como letal-subletal en función de la tolerancia y de la capacidad de rechazo de sedimento por parte de los corales; no obstante, la ausencia de mortalidad coralina, en respuesta a los niveles de sedimentación registrados durante la época de lluvias, y el desarrollo coralino observado en la región pudiera estar relacionado al efecto combinado de: a) la eficiencia de la remoción activa de sedimento, b) el posible incremento en la tolerancia fisiológica al sedimento por parte de los corales pétreos de Bahías de Huatulco, y c) la remoción pasiva de sedimentos vía la turbulencia de la zona. No obstante, el efecto combinado de la sedimentación natural aunado a la sedimentación resultado de actividades antropogénicas en la región, podría promover un cambio en la estructura arrecifal provocando la eventual pérdida de las comunidades coralinas en Bahías de Huatulco.