Tumor treating fields as novel combination partner in the multimodal treatment of head and neck cancer.

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.

Human mesenchymal stromal cells maintain their stem cell traits after high-LET particle irradiation - Potential implications for particle radiotherapy and manned space missions.

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.

Human mesenchymal stem cells are resistant to UV-B irradiation.

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.

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry.

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.

Mesenchymal stem cells preserve their stem cell traits after exposure to antimetabolite chemotherapy.

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.

DNA damage response of clinical carbon ion versus photon radiation in human glioblastoma cells.

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.

The Therapeutic Potential of Mesenchymal Stromal Cells in the Treatment of Chemotherapy-Induced Tissue Damage.

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.

The current understanding of mesenchymal stem cells as potential attenuators of chemotherapy-induced toxicity.

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.

Human mesenchymal stem cells lose their functional properties after paclitaxel treatment.

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.

Radiation-induced pulmonary gene expression changes are attenuated by the CTGF antibody Pamrevlumab.

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.

Superresolution light microscopy shows nanostructure of carbon ion radiation-induced DNA double-strand break repair foci.

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 ∼100 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.

Mesenchymal stem cells maintain their defining stem cell characteristics after treatment with cisplatin.

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.

Radio-resistant mesenchymal stem cells: mechanisms of resistance and potential implications for the clinic.

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.

Mesenchymal stem cells ­ A new hope for radiotherapy-induced tissue damage?

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.

Mesenchymal stem cells are resistant to carbon ion radiotherapy.

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.

Ophiuroidea (Echinodermata) from coral reefs in the Mexican Pacific.

There are numerous and important coral reefs in the Mexican Pacific, but scarce studies of brittle stars conducted in these ecosystems. In this regard, this work provides the first annotated checklist of brittle stars associated with coral communities and reefs in the Mexican Pacific and an illustrated key to identify the species. We also provide taxonomic descriptions, spatial and bathymetric distributions and some important remarks of the species. We report a total of 14 species of brittle stars belonging to nine genera and seven families. Ophiocnida hispida in Jalisco, Ophiophragmus papillatus in Guerrero, and Ophiothrix (Ophiothrix) spiculata and Ophiactis simplex in Colima are new distribution records. The record of O. papillatus is remarkable because the species has not been reported since its description in 1940. The brittle stars collected in this study, represent 22.2% of the total species previously reported from the Mexican Pacific. Presently, anthropogenic activities on the coral reefs of the Mexican Pacific have increased, thus the biodiversity of brittle stars in these ecosystems may be threatened.

Testing the genetic predictions of a biogeographical model in a dominant endemic Eastern Pacific coral (Porites panamensis) using a genetic seascape approach.

The coral fauna of the Eastern Tropical Pacific (ETP) is depauperate and peripheral; hence, it has drawn attention to the factors allowing its survival. Here, we use a genetic seascape approach and ecological niche modeling to unravel the environmental factors correlating with the genetic variation of Porites panamensis, a hermatypic coral endemic to the ETP. Specifically, we test if levels of diversity and connectivity are higher among abundant than among depauperate populations, as expected by a geographically relaxed version of the Abundant Center Hypothesis (rel-ACH). Unlike the original ACH, referring to a geographical center of distribution of maximal abundance, the rel-ACH refers only to a center of maximum abundance, irrespective of its geographic position. The patterns of relative abundance of P. panamensis in the Mexican Pacific revealed that northern populations from Baja California represent its center of abundance; and southern depauperate populations along the continental margin are peripheral relative to it. Genetic patterns of diversity and structure of nuclear DNA sequences (ribosomal DNA and a single copy open reading frame) and five alloenzymatic loci partially agreed with rel-ACH predictions. We found higher diversity levels in peninsular populations and significant differentiation between peninsular and continental colonies. In addition, continental populations showed higher levels of differentiation and lower connectivity than peninsular populations in the absence of isolation by distance in each region. Some discrepancies with model expectations may relate to the influence of significant habitat discontinuities in the face of limited dispersal potential. Environmental data analyses and niche modeling allowed us to identify temperature, water clarity, and substrate availability as the main factors correlating with patterns of abundance, genetic diversity, and structure, which may hold the key to the survival of P. panamensis in the face of widespread environmental degradation.

Sedimentación en comunidades arrecifales de Bahías de Huatulco, Oaxaca, México

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.

[Sedimentation on reef communities at Bahías de Huatulco, Oaxaca, Mexico]. / Sedimentación en comunidades arrecifales de Bahías de Huatulco, Oaxaca, México.

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 (F,36 = 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) year(-1)), intermediate at San Agustin, 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 Bahiás de Huatulco.