Advances in methods to analyse cardiolipin and their clinical applications

Cardiolipin (CL) is a mitochondria-exclusive phospholipid, primarily localised within the inner mitochondrial membrane, that plays an essential role in mitochondrial architecture and function. Aberrant CL content, structure, and localisation have all been linked to impaired mitochondrial activity and are observed in the pathophysiology of cancer and neurological, cardiovascular, and metabolic disorders. The detection, quantification, and localisation of CL species is a valuable tool to investigate mitochondrial dysfunction and the pathophysiological mechanisms underpinning several human disorders. CL is measured using liquid chromatography, usually combined with mass spectrometry, mass spectrometry imaging, shotgun lipidomics, fluorometry, and radiolabelling. This review summarises available methods to analyse CL, with a particular focus on modern mass spectrometry, and evaluates their advantages and limitations. We provide guidance aimed at selecting the most appropriate technique, or combination of techniques, when analysing CL in different model systems, and highlight the clinical contexts in which measuring CL is relevant

Feeding on intertidal microbial mats by postlarval tiger shrimp, Penaeus semisulcatus De Haan

A series of experiments investigated the potential role of microbial mats in nutrition of the early settlement stages of Penaeus semisulcatus. From 3 days post-metamorphosis, the microbial mat supported high growth and survival rates in postlarvae, equivalent to that supported by a control diet of Artemia nauplii and mussel. Examination of gut contents indicated that benthic postlarvae feed indiscriminately on the microbial mat. However, when postlarvae were fed separated size-fractions of the microbial mat, only the fraction containing a high concentration of infauna (mainly nematodes) was able to support the same growth as intact microbial mat. This appears to be due to the low nitrogen content (0.4-0.9 mmol g-1) of the various size-fractions, compared to that of infauna (4.0 mmol g-1). The stable isotope composition of the dietary size-fractions and postlarval shrimp tissue supports the hypothesis that the shrimp assimilated C and N primarily from the associated infauna. This may be due to selective feeding that is not apparent from stomach contents, due to rapid digestion of fauna soft tissues, or to differential assimilation of infaunal prey relative to other microbial mat components. The results demonstrate that microbial mats may support survival and growth in early-stage penaeid shrimp postlarvae on intertidal mud flats

Evidence for Hydroxyl Radical Scavenging Action of Nitric Oxide Donors in the Protection Against 1-Methyl-4-phenylpyridinium-induced Neurotoxicity in Rats

In the present study we provide evidence for hydroxyl radical (•OH) scavenging action of nitric oxide (NO•), and subsequent dopaminergic neuroprotection in a hemiparkinsonian rat model. Reactive oxygen species are strongly implicated in the nigrostriatal dopaminergic neurotoxicity caused by the parkinsonian neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). Since the role of this free radical as a neurotoxicant or neuroprotectant is debatable, we investigated the effects of some of the NO• donors such as S-nitroso-N-acetylpenicillamine (SNAP), 3-morpholinosydnonimine hydrochloride (SIN-1), sodium nitroprusside (SNP) and nitroglycerin (NG) on in vitro •OH generation in a Fenton-like reaction involving ferrous citrate, as well as in MPP+-induced •OH production in the mitochondria. We also tested whether co-administration of NO• donor and MPP+ could protect against MPP+-induced dopaminergic neurotoxicity in rats. While NG, SNAP and SIN-1 attenuated MPP+-induced •OH generation in the mitochondria, and in a Fenton-like reaction, SNP caused up to 18-fold increase in •OH production in the latter reaction. Striatal dopaminergic depletion following intranigral infusion of MPP+ in rats was significantly attenuated by NG, SNAP and SIN-1, but not by SNP. Solutions of NG, SNAP and SIN-1, exposed to air for 48 h to remove NO•, when administered similarly failed to attenuate MPP+-induced neurotoxicity in vivo. Conversely, long-time air-exposed SNP solution when administered in rats intranigrally, caused a dose-dependent depletion of the striatal dopamine. These results confirm the involvement of •OH in the nigrostriatal degeneration caused by MPP+, indicate the •OH scavenging ability of NO•, and demonstrate protection by NO• donors against MPP+-induced dopaminergic neurotoxicity in rats

Respiration mitochondriale, données de base

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