Spatial distribution and characteristics of plastic pollution in the salt marshes of Bahía Blanca Estuary, Argentina.

This study delves into the magnitude and attributes of plastic pollution in the salt marshes of the Bahía Blanca Estuary, Argentina, with a specific focus on its spatial distribution. The investigation included the evaluation of microplastics (1-5 mm), mesoplastics (5-25 mm) and macroplastics (25-100 mm), discovering elevated levels along the high salt marsh strandline compared to low salt marsh and mudflat areas. Notably, the abundance of plastic reached staggering levels, reaching up to 20,060 items/m2 in the vicinity of an illegal dumpsite. Microplastics, particularly in the 2-4 mm range, were dominant, and the main plastic components were high-density polyethylene (HDPE), low-density polyethylene (LDPE), polypropylene (PP), and polystyrene (PS). Plastic films emerged as the predominant plastic type, while the presence of pellets hinted at potential sources such as illegal dumping and port-related activities. This contamination could be largely attributed to inappropriate waste management practices and urban runoff, which pose a substantial ecological threat to these ecosystems. Urgent remedial action is essential to protect these marshes, underscoring the critical need for comprehensive wetland management and educational initiatives to ensure their long-term sustainability.

High passage numbers induce resistance to apoptosis in C2C12 muscle cells.

Cell lines with high passage numbers exhibit alterations in cell morphology and functions. In the present work, C2C12 skeletal muscle cells with either low (< 20) or high (> 60) passage numbers (identified as 1-C2C12 or h-C2C12, respectively) were used to investigate the apoptotic response to H2O2 as a function of culture age h-C2C12. We found that older cultures (h-C2C12 group) were depleted of mitochondrial DNA (mtDNA). When we analyzed the behavior of Bad, Bax, caspase-3 and mitochondrial transmembrane potential, we observed that cells in the h-C2C12 group were resistant to H2O2 induction of apoptosis. We propose serially cultured C2Cl2 cells as a refractory model to H2O2-induced apoptosis. In addition, the data obtained in this work suggest that mtDNA is required for apoptotic cell death in skeletal muscle C2C12 cells.

Microplastic levels on sandy beaches: Are the effects of tourism and coastal recreation really important?

This study assessed the effect of tourism and other recreational activities on microplastic (MP) levels and their characteristics in the sand and surf zone of the seawater. Six sites were chosen belonging to three sandy beaches with similar geomorphologic and morphodynamic characteristics but with different tourism activities. On average, a concentration of 1133.3 ± 811.3 items/kg dry weight (d.w.) and 12.7 ± 14.9 items/m3 were found in the sand and seawater samples, respectively. Fibers and films predominated and were less than 1 mm in length. In the sand, the films mainly matched the PE polymer spectra and the fibers matched PET polymer, cotton, and indigo blue dye; in the seawater samples, PP films and PET fibers prevailed. At the Pehuén-Co - Monte Hermoso Coastal Marine MPA where the flow of tourists is low, the MP levels were the lowest and the largest particles were found, mainly blue or black fibers, with less polymer diversity, cotton and PET being the most prevalent suggesting a recent input of textile fibers to this site. Moreover, the highest concentration of MPs was found on the southern site of a beach considered to be more pristine due to negligible human activity, including the smallest size pattern, mostly composed of white films or fibers with a greater diversity of polymers, predominantly PE > PET > PP. A great occurrence of PVC white films was also found in the surf zone at this site. Proximity to the mouth of a river, littoral drift, and other point sources were identified as the main sources, indicating that, apart from the local tourism and recreational activities, other sources might play a major role in the input of MPs to sandy beaches, such as extensive/intensive agricultural land use and irrigation areas.

First evidence of microplastics in nine lakes across Patagonia (South America).

Microplastics (MPs) on lakes have been reported mainly from Europe, Asia, and North America. Then, this study aimed to address the quantification and identification of MPs in nine lakes from the Argentine Patagonian Region. Blue colored fibers were dominant, with a size range between 0.2 and <0.4 mm. The mean MPs concentration was 0.9 ± 0.6 MPs m-3, suggesting a low pollution state when compared to other worldwide lakes. Raman microscopy analysis showed a predominance of Indigo Blue Polyethylene terephthalate (PET) particles. The upper-gradient runoff from urban settlements, textiles, and fisheries were identified as the main MPs sources and levels positively correlated with the higher area, shallower depth, and with an end-position in the watershed. These findings fill a gap in the geographical distribution knowledge, setting a baseline that emphasizes the need for better treatment of urban and fisheries wastes in continental lakes.

Role of 17ß-estradiol and testosterone in apoptosis.

17ß-Estradiol (E2) and Testosterone (T) exert actions in most animal tissues, in addition to the reproductive system. Thus, both sex steroid hormones affect growth and different cell functions in several organs. Accordingly, the nuclear estrogen (ER) and androgen (AR) receptors are ubiquitously expressed. Moreover, ER and AR may have non-classical intracellular localizations, e.g. plasma membrane, mitochondria and endoplasmic reticulum, raising additional complexity to the functional roles of E2 and T. In addition to the modulation of gene transcription by direct interaction with their cognate nuclear receptors, the steroids can rapidly activate signaling pathways by a non-genomic mechanism mediated by receptors identical to or different from known steroid receptors. Among various functions, E2 and T can regulate apoptosis through those pathways. In mitochondria, the presence of ER and AR and actions of estrogen and androgen have been shown, in keeping with the organelle being a control point of apoptosis. The most recurrent action for each steroid hormone is the protection of mitochondria against different insults, resulting in antiapoptosis. This review summarizes the molecular basis of the modulation of programmed cell death by E2 and T in several tissues.

Extracellular-regulated kinase and p38 mitogen-activated protein kinases are involved in the antiapoptotic action of 17beta-estradiol in skeletal muscle cells.

17beta-Estradiol (E(2)) stimulates the mitogen-activated protein kinases (MAPKs) in various cellular types. We have shown that the hormone activates extracellular-regulated kinase (ERK) and p38 MAPK in skeletal muscle cells. However, the functions of MAPK modulation by the estrogen in muscle cells have not been studied yet. We have recently reported antiapoptotic actions of E(2) in C2C12 cells. Here, the role of MAPKs mediating the hormone effect in muscle cells was investigated. The results showed that cells exposed to 0.5 mM hydrogen peroxide (H(2)O(2)) presented cytoskeleton disorganization, mitochondrial redistribution, and picnotic/fragmented nuclei. Pretreatment with 10(-8) M E(2) prevented these morphological apoptotic characteristics, except in the presence of ERK or p38 MAPK inhibitors, U0126 and SB203580 respectively. Mitochondrial membrane integrity was also studied. Preincubation of cultures with 10(-8) M E(2) abrogated H(2)O(2) effects such as Janus Green oxidation, presence of cytochrome c oxidase activity in the cytoplasm, and SMAC/DIABLO release from mitochondria. When MAPKs were inhibited, the hormone could not prevent mitochondrial membrane damage exerted by oxidative stress. Blocking experiments with small interfering RNAs confirmed that both ERK and p38 MAPKs mediate the antiapoptotic effects of the hormone at the mitochondrial level. Further, some of the molecular mechanisms involved were also investigated. Thus, E(2) was able to induce AKT (Ser473) and BAD (Ser112) phosphorylation in C2C12 cells in the absence or in the presence of H(2)O(2) but not when the cultures were incubated with H(2)O(2) and MAPK inhibitors. Altogether, these results show that E(2) exerts a survival action in skeletal muscle cells involving ERK and p38 MAPK activation.

High passage numbers induce resistance to apoptosis in C2C12 muscle cells

Cell lines with high passage numbers exhibit alterations in cell morphology and functions. In the present work, C2C12 skeletal muscle cells with either low (<20) or high (>60) passage numbers (identified as l-C2C12 or h-C2C12, respectively) were used to investigate the apoptotic response to H2O2 as a function of culture age h-C2C12. We found that older cultures (h-C2C12 group) were depleted of mitochondrial DNA (mtDNA). When we analyzed the behavior of Bad, Bax, caspase-3 and mitochondrial transmembrane potential, we observed that cells in the h-C2C12 group were resistant to H2O2 induction of apoptosis. We propose serially cultured C2C12 cells as a refractory model to H2O2-induced apoptosis. In addition, the data obtained in this work suggest that mtDNA is required for apoptotic cell death in skeletal muscle C2C12 cells.

Rol protector del 17ß-Estradiol y la testosterona en la apoptosis del músculo esquelético / Protective role of 17ß-Estradiol and testosterone in apoptosis of skeletal muscle

La sarcopenia, pérdida de masa y fuerza del músculo esqueléico, es una condición frecuente durante el envejecimiento. Conduce a incapacidad motora resultando en internación y mortalidad. Puesto que los niveles de estrógenos y/o testosterona disminuyen con la edad, la sarcopenia se ha asociado al déficit de estas hormonas. Aunque los mecanismos moleculares involucrados en esta patología no están totalmente dilucidados, existen evidencias indicando que la apoptosis es en parte responsable de la pérdida de miocitos en la adultez. Previamente demostramos que el 17ß-estradiol (E2) inhibe la apoptosis en la línea celular C2C12 de músculo esquelético a través de PI3K/Akt, MAPKs, HSP27 y receptores estrogénicos (ERs) con localización no clásica. Usando siRNAs específicos para silenciar las isoformas del ER, comprobamos que el E2 activa ERK involucrando a ERa, mientras que la activación de p38 MAPK es independiente de ERs. Confirmamos que el E2 puede inhibir la apoptosis a través de las MAPKs en cultivos primarios de músculo esquelético de ratón. Al igual que la E2, la testosterona bloquea la apoptosis. Las alteraciones morfológicas típicas de la apoptosis como fragmentación nuclear, desorganización del citoesqueleto, reorganización/disfunción mitocondrial y liberación de citocromo c, inducidos por H2O2 fueron suprimidas al preincubar las células con testosterona. Se requieren investigaciones adicionales para establecer un paralelismo entre los mecanismos de acción de ambas hormonas, que podrían estar implicados en patologías musculares asociadas a apoptosis. Los datos presentados en este estudio profundizan el conocimiento de las bases moleculares de la sarcopenia relacionada con estados de déficit de hormonas sexuales.