Trimethylamine N-oxide does not impact viability, ROS production and mitochondrial membrane potential of adult rat cardiomyocytes

Trimethylamine N-oxide (TMAO) is an organic compound derived from dietary choline and L-carnitine. It behaves as an osmolyte, a protein stabilizer, and an electron acceptor, showing different biological functions in different animals. Recent works point out that, in humans, high circulating levels of TMAO are related to the progression of atherosclerosis and other cardiovascular diseases. However, studies on a direct role of TMAO in cardiomyocyte parameters are still limited. The purpose of this work is to study the effects of TMAO on isolated adult rat cardiomyocytes. TMAO in both 100 µM and 10 mM concentrations, from 1 to 24 h of treatment, does not affect cell viability, sarcomere length, intracellular ROS, and mitochondrial membrane potential. Furthermore, the simultaneous treatment with TMAO and known cardiac insults, such as H2O2 or doxorubicin, does not affect the treatment’s effect. In conclusion, TMAO cannot be considered a direct cause or an exacerbating risk factor of cardiac damage at the cellular level in acute conditions

Trimethylamine N-Oxide (TMAO) Impairs Purinergic Induced Intracellular Calcium Increase and Nitric Oxide Release in Endothelial Cells

Trimethylamine N-oxide (TMAO) is a diet derived compound directly introduced through foodstuff, or endogenously synthesized from its precursors, primarily choline, L-carnitine, and ergothioneine. New evidence outlines high TMAO plasma concentrations in patients with overt cardiovascular disease, but its direct role in pathological development is still controversial. The purpose of the study was to evaluate the role of TMAO in affecting key intracellular factors involved in endothelial dysfunction development, such as reactive oxygen species, mitochondrial health, calcium balance, and nitric oxide release using bovine aortic endothelial cells (BAE-1). Cell viability and oxidative stress indicators were monitored after acute and prolonged TMAO treatment. The role of TMAO in interfering with the physiological purinergic vasodilatory mechanism after ATP stimulation was defined through measurements of the rise of intracellular calcium, nitric oxide release, and eNOS phosphorylation at Ser1179 (eNOSSer1179). TMAO was not cytotoxic for BAE-1 and it did not induce the rise of reactive oxygen species and impairment of mitochondrial membrane potential, either in the basal condition or in the presence of a stressor. In contrast, TMAO modified the purinergic response affecting intracellular ATP-induced calcium increase, nitric oxide release, and eNOSSer1179. Results obtained suggest a possible implication of TMAO in impairing the endothelial-dependent vasodilatory mechanism

Longitudinal beam dynamics in the Frascati DAΦNE e^{+}e^{-} collider with a passive third harmonic cavity in the lengthening regime

A high-harmonic rf system is going to be installed in both rings of the DAΦNE Φ-Factory collider to improve the Touschek lifetime. The main goal of this paper is to study the impact of the 3rd harmonic cavity on beam dynamics making a special emphasis on the dynamics of a bunch train with a gap. The shift of the coherent synchrotron frequencies of the coupled-bunch modes has been estimated. In the following we investigated the effect of magnification of the synchrotron phase spread and beam spectrum variation due to the gap. Besides we simulated the bunch lengthening for different bunches along the unevenly filled train and evaluated the Touschek lifetime enhancement taking into account the obtained bunch distributions. Finally, the "cavity parking" option is discussed. It can be considered as a reliable backup procedure consisting of tuning the cavity away from the 3rd harmonic frequency and in between two revolution harmonics. It allows recovering, approximately, the same operating conditions as were before the harmonic cavity installation

L'agente OO-Garlic in missione: contro la sindrome metabolica

Ciao, sono il Signor Garlic (ma per gli amici sono l’Agente 00-Garlic). I miei antenati erano molto tristi per via del loro odore cattivo che teneva tutti lontano. Per fortuna con il tempo gli scienziati hanno scoperto che nella puzza che circonda noi della stirpe Garlic si nascondono dei superpoteri! I miei poteri aumentano se vengo trasformato e la mia pelle diventa più scura, infatti inizio a produrre tanto H2S che è un’arma speciale contro i nemici più forti. Così chi è a conoscenza delle fortissime proprietà che possiedo, mi chiama in aiuto per sconfiggere nemici molto cattivi per la salute. Uno dei più grandi nemici per tutti noi si chiama sindrome metabolica... Continua a leggere..

L'agente OO-Garlic in missione: contro la sindrome metabolica

Ciao, sono il Signor Garlic (ma per gli amici sono l’Agente 00-Garlic). I miei antenati erano molto tristi per via del loro odore cattivo che teneva tutti lontano. Per fortuna con il tempo gli scienziati hanno scoperto che nella puzza che circonda noi della stirpe Garlic si nascondono dei superpoteri! I miei poteri aumentano se vengo trasformato e la mia pelle diventa più scura, infatti inizio a produrre tanto H2S che è un’arma speciale contro i nemici più forti. Così chi è a conoscenza delle fortissime proprietà che possiedo, mi chiama in aiuto per sconfiggere nemici molto cattivi per la salute. Uno dei più grandi nemici per tutti noi si chiama sindrome metabolica... Continua a leggere..

Protective Effects of (E)-β-Caryophyllene (BCP) in Chronic Inflammation

(E)-β-caryophyllene (BCP) is a bicyclic sesquiterpene widely distributed in the plant kingdom, where it contributes a unique aroma to essential oils and has a pivotal role in the survival and evolution of higher plants. Recent studies provided evidence for protective roles of BCP in animal cells, highlighting its possible use as a novel therapeutic tool. Experimental results show the ability of BCP to reduce pro-inflammatory mediators such as tumor necrosis factor-alfa (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), thus ameliorating chronic pathologies characterized by inflammation and oxidative stress, in particular metabolic and neurological diseases. Through the binding to CB2 cannabinoid receptors and the interaction with members of the family of peroxisome proliferator-activated receptors (PPARs), BCP shows beneficial effects on obesity, non-alcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) liver diseases, diabetes, cardiovascular diseases, pain and other nervous system disorders. This review describes the current knowledge on the biosynthesis and natural sources of BCP, and reviews its role and mechanisms of action in different inflammation-related metabolic and neurologic disorders