Portuguese fish producers’ organisations: some concerns

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Anti-tumoral activity of lipophilic Eucalyptus bark extracts, enriched on triterpenic acids, against breast cancer cells

The agro-industrial exploitation of eucalyptus for pulp production generates large amounts of biomass residues, particularly bark. Eucalyptus spp. is the most important fiber source for pulp and paper production in southwestern Europe [1]

Antitumoral and antioxidant activities of lipophilic and phenolic extracts from Cynara cardunculus L. var. altilis (DC)

Cynara cardunculus L. var. altilis (DC) (Cca) grows under the semi-arid conditions as those of south of Portugal. Given to high cellulose and hemicelluloses contents, paper pulp production has been proposed [1]. Moreover, the extraction of bioactive compounds could also be considered for an integrated valorization of Cca. Sesquiterpene lactones (SL) and pentacyclic triterpenes, the major constituents of Cca leaves and capitula lipophilic fractions [2] showed lower tryglyceride levels in rat serum [3] and anti-inflammatory [4] actions, respectively. Besides, cardoon extracts displayed antioxidant [5] and antitumor properties [6, 7], mainly due to hydroxycinnamic acid derivatives. The present work aims to determine the chemical composition of Cca lipophilic and phenolic fractions, by analyzing respectively their dichloromethane (DCM) and methanol/water/acetic acid (MWAA) (49.5:49.5:1) extracts, by gas chromatography and high temperature-ultra-high pressure liquid chromatography coupled with mass spectrometry. Furthermore, the antitumoral activity of Cca DCM extracts was evaluated on human breast cancer cells (MDA-MB-231), by assessing cell proliferation (2 – 500 µg/mL), cell cycle and Akt molecular signaling (10.4 µg/mL). Additionally, the antioxidant activity of MWAA extracts (7.5 – 400 µg/mL) was determined by DPPH scavenging assay. Cca leaves DCM extract, containing 48.5 ± 3.1% SLs (Table 1), and the major compound, cynaropicrin (2), strongly inhibited MDA-MB-231 cellular viability, inducing cell cycle arrest at G2 phase, with inhibition of Akt phosphorylation at serine 473. In addition, MWAA extracts from Cca stalks outer part, containing 5.9 ± 0.5% hydroxycinnamic acids (HA), were the most effective to scavenge DPPH free radicals. The antioxidant activity was correlated to phenolic (r =-0.897) and HAs (r =-0.990) contents. In conclusion, Cca leaves and stalks outer part are valuable sources of respectively SLs and HAs, with a great antitumoral and antioxidant potential

Cholesteryl Hemiazelate Present in Cardiovascular Disease Patients Causes Lysosome Dysfunction in Murine Fibroblasts

Funding Information: This work was financially supported by the FCT (Foundation for Science and Technology of the Portuguese Ministry of Science and Higher Education), Refs. 2022.01305.PTDC and 2022.03249.PTDC. The Coimbra Chemistry Centre (CQC) is supported by the FCT through projects UIDB/00313/2020 and UIDP/00313/2020. E.L. is the holder of a PhD fellowship from the FCT (2021.06265.BD). A.R.A.M. was funded by the FCT Stimulus of Scientific Employment Individual Support Call 2017 (CEECIND/01006/2017). R.P. was funded by the NHLBI Division of Intramural Research (ZIA HL006151-10). Publisher Copyright: © 2023 by the authors.There is growing evidence supporting the role of fibroblasts in all stages of atherosclerosis, from the initial phase to fibrous cap and plaque formation. In the arterial wall, as with macrophages and vascular smooth muscle cells, fibroblasts are exposed to a myriad of LDL lipids, including the lipid species formed during the oxidation of their polyunsaturated fatty acids of cholesteryl esters (PUFA-CEs). Recently, our group identified the final oxidation products of the PUFA-CEs, cholesteryl hemiesters (ChE), in tissues from cardiovascular disease patients. Cholesteryl hemiazelate (ChA), the most prevalent lipid of this family, is sufficient to impact lysosome function in macrophages and vascular smooth muscle cells, with consequences for their homeostasis. Here, we show that the lysosomal compartment of ChA-treated fibroblasts also becomes dysfunctional. Indeed, fibroblasts exposed to ChA exhibited a perinuclear accumulation of enlarged lysosomes full of neutral lipids. However, this outcome did not trigger de novo lysosome biogenesis, and only the lysosomal transcription factor E3 (TFE3) was slightly transcriptionally upregulated. As a consequence, autophagy was inhibited, probably via mTORC1 activation, culminating in fibroblasts’ apoptosis. Our findings suggest that the impairment of lysosome function and autophagy and the induction of apoptosis in fibroblasts may represent an additional mechanism by which ChA can contribute to the progression of atherosclerosis.publishersversionpublishe