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Mata Cabana, A.

Publications and source records attributed to Mata Cabana, A..

2 recordsLinked to original sources

Methanolic extracts of the edible halophyte Crithmum maritimum enhance oxidative stress resistance in Caenorhabditis elegans through hormetic mechanisms

Halophytes are promising sources of bioactive phenolic compounds for the food and pharmaceutical industries. However, their phenolic composition is influenced by environmental conditions, and the in vivo antioxidant activity of their phytochemicals is largely unknown. We evaluated the antioxidant capacity of phenolic-rich methanolic extracts from the edible halophyte Crithmum maritimum, grown in wild and greenhouse conditions. Additionally, their in vivo antioxidant capacity was analyzed for the first time using the model Caenorhabditis elegans. Wild plant extracts showed higher phenolic content and diversity, and in vitro antioxidant activity. Both extracts enhanced oxidative stress resistance and increased nematode survival rates, albeit to varying extents, and increased reactive oxygen species production in nematodes, without affecting their lifespan, suggesting a hormetic mechanism. Although no neuroprotective effects were observed in models of neurodegenerative diseases, these findings highlight the potential of C. maritimum as a valuable source of phenolics with antioxidant properties for the food industry.

pharmacology and toxicology↗

Prolonged quiescence delays somatic stem cell-like division in Caenorhabditis elegans and is controlled by insulin signalling

Cells can enter quiescence in adverse conditions and resume proliferation when the environment becomes favourable. Prolonged quiescence comes with a cost, reducing proliferation potential and survival. Interestingly, cellular quiescence also occurs in normal development, with many cells spending most of their lifetime at this state. Elucidating the mechanisms involved in surviving long-term quiescence and in maintenance of cellular proliferation potential will contribute to a better understanding of the process of tissue regeneration. Developmental arrest of C. elegans at the L1 stage is an emerging model for the study of cellular quiescence and reactivation. During arrest, L1 larvae undergo a process that shares phenotypic hallmarks with the ageing of the adult. Interestingly, insulin signalling, a prominent pathway in the regulation of ageing, also balances cell proliferation and activation of stress resistance pathways during quiescence, becoming a candidate regulator of proliferation potential. Here we report that prolonged L1 quiescence delays reactivation of blast cell divisions in C. elegans, leading to a delay in the initiation of postembryonic development. This delay is accompanied by increased inter-individual variability. We propose that the delay in cell division results from the decline that animals suffer during L1 arrest. To that end, we show that insulin signalling modulates the rate of L1 ageing, affecting proliferative potential after quiescence. These findings support that the insulin signalling pathway has a comparable role in L1 arrest to that in ageing adults. Furthermore, we show that variable yolk provisioning to the embryos as a consequence of maternal age is one of the sources of inter-individual variability in recovery after quiescence of genetically identical animals. Taken together, these results support the relevance of L1 arrest as a model to study in vivo proliferation after quiescence and to understand the mechanisms for maintenance of proliferation potential.

developmental biology↗