Search

Background: Infertility is a major health issue, affecting 15% of reproductive‐age couples with male factors contributing to 50% of cases. Asthenozoospermia (AS), or low sperm motility, is a common cause of male infertility with complex aetiology, involving genetic and metabolic alterations, inflammation and oxidative stress. However, the molecular mechanisms behind low motility are unclear. In this study, we used a metabolomics approach to identify metabolic biomarkers and pathways involved in sperm motility. Methods: We compared the metabolome and lipidome of spermatozoa of men with normozoospermia (n = 44) and AS (n = 22) using untargeted LC–MS and the metabolome of seminal fluid using 1H‐NMR. Additionally, we evaluated the seminal fluid redox status to assess the oxidative stress in the ejaculate. Results: We identified 112 metabolites and 209 lipids in spermatozoa and 27 metabolites in the seminal fluid of normozoospermic and asthenozoospermic men. PCA analysis of the spermatozoa's metabolomics and lipidomics data showed a clear separation between groups. Spermatozoa of asthenozoospermic men presented lower levels of several amino acids, and increased levels of energetic substrates and lysophospholipids. However, the metabolome and redox status of the seminal fluid was not altered inAS. Conclusions: Our results indicate impaired metabolic pathways associated with redox homeostasis and amino acid, energy and lipid metabolism in AS. Taken together, these findings suggest that the metabolome and lipidome of human spermatozoa are key factors influencing their motility and that oxidative stress exposure during spermatogenesis or sperm maturation may be in the aetiology of decreased motility in AS. [ABSTRACT FROM AUTHOR]

Dunaliella salina is a green microalga extensively explored for β-carotene production, while knowledge of its lipid composition is still limited and poorly investigated. Among lipids, polar lipids have been highlighted as bioactive phytochemicals with health-promoting properties. This research aimed to provide an in-depth lipidome profiling of D. salina using liquid and gas chromatography coupled with mass spectrometry. The lipid content was 6.8%, including phospholipids, glycolipids, betaine lipids, sphingolipids, triglycerides, diglycerides, and pigments. Among the total esterified fatty acids, 13.6% were 18:3 omega-3 and 14.7% were 18:1 omega-9. The lipid extract of D. salina showed anti-inflammatory activity by inhibiting cyclooxygenase-2 activity at 100 µg/mL, dose-dependent antioxidant scavenging activity, and antidiabetic activity by inhibiting α-glucosidase activity at 25 and 125 µg/mL. In conclusion, the lipid extract of D. salina has the potential to be used as a functional food ingredient or in the nutraceutical and cosmeceutical industries. [ABSTRACT FROM AUTHOR]

Elysia crispata (Sacoglossa, Gastropoda) is a tropical sea slug known for its ability to incorporate functional chloroplasts from a variety of green macroalgae, a phenomenon termed kleptoplasty. This sea slug, amenable to laboratory cultivation, produces mucus, a viscous secretion that serves diverse purposes including protection, locomotion, and reproduction. In this study, we profiled the antimicrobial, antioxidant, and anti-inflammatory activities of the mucus of this sea slug. Results revealed inhibitory activity against several bacterial strains, more pronounced for Gram–negative bacteria. Particularly interesting was the strong inhibitory effect against Pseudomonas aeruginosa, a bacterial species classified by the WHO as a high-priority pathogen and associated with high-risk infections due to its frequent multidrug-resistant profile. Similar inhibitory effects were observed for the mucus native protein extracts, indicating that proteins present in the mucus contributed significantly to the antimicrobial activity. The mucus also showed both antioxidant and anti-inflammatory activities. The latter activities were associated with the low molecular weight (<10 kDa) fraction of the mucus rather than the native protein extracts. This study opens the way to further research on the biotechnological applications of the mucus secreted by this unique marine organism, particularly as an antimicrobial agent. [ABSTRACT FROM AUTHOR]

Psoriasis is characterized by excessive exfoliation of the epidermal layer due to enhanced pro-inflammatory signaling and hyperproliferation of keratinocytes, further modulated by UV-based anti-psoriatic treatments. Consequently, this study aimed to evaluate the impact of a lipid extract derived from the microalgae Nannochloropsis oceanica on the proteomic alterations induced by lipid derivatives in non-irradiated and UVB-irradiated keratinocytes from psoriatic skin lesions compared to keratinocytes from healthy individuals. The findings revealed that the microalgae extract diminished the viability of psoriatic keratinocytes without affecting the viability of these cells following UVB exposure. Notably, the microalgae extract led to an increased level of 4-HNE-protein adducts in non-irradiated cells and a reduction in 4-hydroxynonenal (4-HNE)-protein and 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2)-protein adducts in UVB-exposed keratinocytes from psoriasis patients. In healthy skin cells, the extract decreased the UV-induced elevation of 4-HNE-protein and 15d-PGJ2-protein adducts. The antioxidant/anti-inflammatory attributes of the lipid extract from the Nannochloropsis oceanica suggest its potential as a protective agent for keratinocytes in healthy skin against UVB radiation's detrimental effects. Moreover, it could offer therapeutic benefits to skin cells afflicted with psoriatic lesions by mitigating their proliferation and inflammatory responses during UV radiation treatment. [ABSTRACT FROM AUTHOR]

Phosphatidylethanolamine (PE) and phosphatidylserine (PS), along with phosphatidylcholine (PC), are key phospholipids (PL) in cell membranes and lipoproteins, prone to oxidative modifications. Their oxidized forms, OxPE and OxPS, play significant roles in inflammation and immune response. This review explores their structural oxidative changes under non‐enzymatic conditions and their roles in physiological and pathological contexts, influencing inflammation, and immunity. Specific oxidations of PE and PS significantly alter their physicochemical properties, leading to enhanced biological functions, reduced activity, or inactivation. OxPE may show pro‐inflammatory actions, similar to well‐documented OxPC, while the OxPS pro‐inflammatory effects are less noted. However, OxPS and OxPE have also shown an antagonistic effect against lipopolysaccharides (LPS), suggesting a protective role against exacerbated immune responses, similar to OxPC. Further research is needed to deepen our understanding of these less‐studied OxPL classes. The role of OxPE and OxPS in disease pathogenesis remains largely unexplored, with limited studies linking them to Alzheimer's disease, diabetes, rheumatoid arthritis, traumatic brain injury, and skin inflammation. These findings highlight the potential of OxPE and OxPS as biomarkers for disease diagnosis, monitoring, and therapeutic targeting. [ABSTRACT FROM AUTHOR]

Medium‐chain acyl‐CoA dehydrogenase deficiency (MCADD) is the most prevalent mitochondrial fatty acid β‐oxidation disorder. In this study, we assessed the variability of the lipid profile in MCADD by analysing plasma samples obtained from 25 children with metabolically controlled MCADD (following a normal diet with frequent feeding and under l‐carnitine supplementation) and 21 paediatric control subjects (CT). Gas chromatography–mass spectrometry was employed for the analysis of esterified fatty acids, while high‐resolution C18‐liquid chromatography‐mass spectrometry was used to analyse lipid species. We identified a total of 251 lipid species belonging to 15 distinct lipid classes. Principal component analysis revealed a clear distinction between the MCADD and CT groups. Univariate analysis demonstrated that 126 lipid species exhibited significant differences between the two groups. The lipid species that displayed the most pronounced variations included triacylglycerols and phosphatidylcholines containing saturated and monounsaturated fatty acids, specifically C14:0 and C16:0, which were found to be more abundant in MCADD. The observed changes in the plasma lipidome of children with non‐decompensated MCADD suggest an underlying alteration in lipid metabolism. Therefore, longitudinal monitoring and further in‐depth investigations are warranted to better understand whether such alterations are specific to MCADD children and their potential long‐term impacts. [ABSTRACT FROM AUTHOR]

The disruption of mitochondria‐associated endoplasmic reticulum (ER) membranes (MAMs) plays a relevant role in Alzheimer's disease (AD). MAMs have been implicated in neuronal dysfunction and death since it is associated with impairment of functions regulated in this subcellular domain, including lipid synthesis and trafficking, mitochondria dysfunction, ER stress‐induced unfolded protein response (UPR), apoptosis, and inflammation. Since MAMs play an important role in lipid metabolism, in this study we characterized and investigated the lipidome alterations at MAMs in comparison with other subcellular fractions, namely microsomes and mitochondria, using an in vitro model of AD, namely the mouse neuroblastoma cell line (N2A) over‐expressing the APP familial Swedish mutation (APPswe) and the respective control (WT) cells. Phospholipids (PLs) and fatty acids (FAs) were isolated from the different subcellular fractions and analyzed by HILIC‐LC–MS/MS and GC–MS, respectively. In this in vitro AD model, we observed a down‐regulation in relative abundance of some phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and lysophosphatidylethanolamine (LPE) species with PUFA and few PC with saturated and long‐chain FA. We also found an up‐regulation of CL, and antioxidant alkyl acyl PL. Moreover, multivariate analysis indicated that each organelle has a specific lipid profile adaptation in N2A APPswe cells. In the FAs profile, we found an up‐regulation of C16:0 in all subcellular fractions, a decrease of C18:0 levels in total fraction (TF) and microsomes fraction, and a down‐regulation of 9‐C18:1 was also found in mitochondria fraction in the AD model. Together, these results suggest that the over‐expression of the familial APP Swedish mutation affects lipid homeostasis in MAMs and other subcellular fractions and supports the important role of lipids in AD physiopathology. [ABSTRACT FROM AUTHOR]