Peripheral peroxisomal ß-oxidation engages neuronal serotonin signaling to drive stress-induced aversive memory in C. elegans.

Physiological dysfunction confers negative valence to coincidental sensory cues to induce the formation of aversive associative memory. How peripheral tissue stress engages neuromodulatory mechanisms to form aversive memory is poorly understood. Here, we show that in the nematode C. elegans, mitochondrial disruption induces aversive memory through peroxisomal ß-oxidation genes in non-neural tissues, including pmp-4/very-long-chain fatty acid transporter, dhs-28/3-hydroxylacyl-CoA dehydrogenase, and daf-22/3-ketoacyl-CoA thiolase. Upregulation of peroxisomal ß-oxidation genes under mitochondrial stress requires the nuclear hormone receptor NHR-49. Importantly, the memory-promoting function of peroxisomal ß-oxidation is independent of its canonical role in pheromone production. Peripheral signals derived from the peroxisomes target NSM, a critical neuron for memory formation under stress, to upregulate serotonin synthesis and remodel evoked responses to sensory cues. Our genetic, transcriptomic, and metabolomic approaches establish peroxisomal lipid signaling as a crucial mechanism that connects peripheral mitochondrial stress to central serotonin neuromodulation in aversive memory formation.

Electrochemical sensing of hepatocyte viability.

We investigated the use of amperometric and chronoamperometric methods with a double mediator system and screen-printed electrodes (SPEs) for the electrochemical sensing of hepatocyte viability. Cell counts were determined based on measuring cellular respiration via interaction of electroactive redox mediators. The oxidation currents of chronoamperometric measurement were proportional to the concentrations of ferrocyanide which was produced via interaction of cellular respiration, succinate and ferricyanide. The integrated oxidation charges increased linearly with the density of the cultured primary rat hepatocytes over a range of 1 × 10(5) to 5 × 10(5) cells per well (slope = 1.98 (±0.08) µC per 10(5) cells; R(2) = 0.9969), and the detection limit was 7600 (±300) cells per well based on S/N = 3. Each density of cells was cultured in triple replicates and individual cell samples were evaluated. The results of the cytotoxic effect of the chronoamperometric method are comparable to those of the tetrazolium-based colorimetric assay. The chronoamperometric method with ferricyanide and succinate mediators is an efficient, alternative method for assessing the viability of primary hepatocytes which can be completed in 20 min. Succinate did not provide an efficient electron shuttle between cytosolic respiratory redox activity of cancer cells and extracellular ferricyanide, an effect that may be useful for distinguishing hepatocarcinoma cells from healthy hepatocytes.

Bioactivity comparison of extracts from various parts of common and tartary buckwheats: evaluation of the antioxidant- and angiotensin-converting enzyme inhibitory activities.

BACKGROUND: Buckwheat flour and buckwheat sprouts possess antioxidant properties, and previous studies have reported on buckwheat flour displaying an inhibitory activity for angiotensin-I converting enzyme (ACE). Information is lacking on the bioactivity of other parts of the buckwheat, such as the seed hulls and plant stalks. This study investigates the ACE inhibitory activity and antioxidant activity of various parts of 2 types of buckwheat, namely, common buckwheat (Fagopyrum esculentum Moench) and tartary buckwheat (Fagopyrum tataricum Gaertn). RESULTS: The extract of common hulls extracted using 50% (v/v)-ethanol solvent presented a remarkable inhibitory activity. The value of IC50 is 30 µg ml-1. The extracts of both common and tartary hulls extracted using 50% (v/v)-ethanol solvent demonstrated an antioxidant activity that is superior to that of other extracts. CONCLUSION: This study determined that the ethanolic extract of the hulls of common buckwheat presented more favorable antioxidant and ACE inhibitory abilities. However, the correlation of antioxidant activity and ACE inhibitory activity for all 18 types of extracts is low. The ACE inhibitory activity could have been caused by a synergistic effect of flavonoids or from other unidentified components in the extracts. The ethanolic extract of common hulls demonstrated remarkable ACE inhibitory activity and is worthy of further animal study.