The effect of cooking on the concentrations of phenolic compounds and antioxidant activities in 33 colored-fleshed potatoes genotypes was evaluated. The phenolic profiles, concentrations, and antioxidant activity were evaluated with a liquid chromatography diode array detector coupled to a mass spectrometer with an electrospray ionization interface (HPLC-DAD-ESI-MS/MS). Eleven anthocyanins were detected; in the case of red-fleshed genotypes, these were mainly acyl-glycosides derivatives of pelargonidin, whereas, in purple-fleshed genotypes, acyl-glycosides derivatives of petunidin were the most important. In the case of the purple-fleshed genotypes, the most important compound was petunidin-3-coumaroylrutinoside-5-glucoside. Concentrations of total anthocyanins varied between 1.21 g kg⁻¹ in fresh and 1.05 g kg⁻¹ in cooked potato and the decreases due to cooking ranged between 3% and 59%. The genotypes that showed the highest levels of total phenols also presented the highest levels of antioxidant activity. These results are of relevance because they suggest anthocyanins are important contributors to the antioxidant activity of these potato genotypes, which is significant even after the drastic process of cooking.

In rainy areas, sweet cherries are cultivated under plastic covers, preventing the cracking of the fruit but decreasing the firmness and acidity of the cherries. We evaluated the impact of plastic cover and pre-harvest K foliar application on quality parameters, antioxidant properties, and phenolic and organic acid compositions in fruits of sweet cherry cv. Regina of Southern Chile. Our results showed that K+ increased firmness, total soluble content, size, fruit weight, and titratable acidity at harvest, independent of the cover factor. The positive impacts of foliar K fertilization on anthocyanins, flavonoids, and phenolic acids could explain the higher antioxidant capacity of fruits. Our study revealed that the additional K doses applied increased malic acid, the main organic acid in cherry fruits, but only in fruits from uncovered trees. In covered trees, the effect was reversed. Citric acid was higher in fruit from covered trees. Our results indicated that tartaric acid also increased with the application of higher K doses; however, this acid was detectable only in uncovered tree fruit. Interestingly, all organic acids were lower in fruits produced in the lower canopy than those detected in fruits harvested from the upper canopy. This showed the positive impact of canopy light exposure on maintaining suitable acidity levels in sweet cherry fruits.

Cellular senescence is an irreversible state linked to aging that involves molecular and functional alterations. The mammalian hippocampus, a key brain region for learning and memory, is highly vulnerable to damage in age-related neurodegenerative diseases, yet the role of cellular senescence in hippocampal aging remains underexplored. Here, we report an early onset of senescence signatures in hippocampal astrocytes of the accelerated aging and frailty mouse model SAMP8. We examine how astrocyte senescence affects excitatory synapse formation, focusing on soluble signals released by astrocytes. Astrocytes isolated from SAMP8 brain and those differentiated from SAMP8 neural stem cells show senescence hallmarks (SA-β-gal, p16 ^INK4a , Lamin B1 loss), alongside a significant reduction in synaptogenic function. While astrocyte-conditioned medium (ACM) from control mice promotes excitatory synaptogenesis through thrombospondin-1 / α2δ-1 neuronal receptor signalling, ACM from senescent SAMP8 astrocytes lacks this capacity. Supplementing senescent ACM with thrombospondin-1 protein, or overexpressing thrombospondin-1 gene in senescent astrocytes, reinstates synaptogenesis. At the hippocampal level, thrombospondin-1 and synaptic puncta are reduced in SAMP8 mice. Our findings reveal that senescent astrocytes exhibit reduced synaptogenic capacity due to thrombospondin-1 loss, highlighting their contribution to synaptic dysfunction during aging. Preventing senescence in hippocampal astrocytes may thus restore astrocyte-mediated synaptogenesis in the aged brain.