• Energy Research

Supplementing the diet of ruminants with agro-industrial by-products is a common practice. In this study, we applied an untargeted lipidomics approach to study the changes in the milk lipid metabolite profiles linked to the addition of different doses of spent coffee grounds (SCG) to the diet of lactating goats. The carryover of caffeine from feed to milk was also studied. Compared to controls, the milk of goats on the SCG diet showed higher levels of cholesteryl esters, sphingomyelins, and phospholipids, while nonesterified fatty acids were downregulated. After 12 h from the last SCG dose, the carry-over of caffeine was, on average, 3%. Collectively, our results establish that SCG supplementation induces changes in the milk levels of complex lipid molecules and causes the transfer of caffeine and caffeine metabolites from feed to milk.

Supplementing the diet of ruminants with agro-industrial by-products is a common practice. In this study, we applied an untargeted lipidomics approach to study the changes in the milk lipid metabolite profiles linked to the addition of different doses of spent coffee grounds (SCG) to the diet of lactating goats. The carryover of caffeine from feed to milk was also studied. Compared to controls, the milk of goats on the SCG diet showed higher levels of cholesteryl esters, sphingomyelins, and phospholipids, while nonesterified fatty acids were downregulated. After 12 h from the last SCG dose, the carry-over of caffeine was, on average, 3%. Collectively, our results establish that SCG supplementation induces changes in the milk levels of complex lipid molecules and causes the transfer of caffeine and caffeine metabolites from feed to milk.

Abnormal consumption of ethanol, the ingredient responsible for alcoholic drinks’ addictive liability, causes millions of deaths yearly. Ethanol’s addictive potential is triggered through activation, by a still unknown mechanism, of the mesolimbic dopamine (DA) system, part of a key motivation circuit, DA neurons in the posterior ventral tegmental area (pVTA) projecting to the ipsilateral nucleus accumbens shell (AcbSh). The present in vivo brain microdialysis study, in dually-implanted rats with one probe in the pVTA and another in the ipsilateral or contralateral AcbSh, demonstrates this mechanism. As a consequence of the oral administration of a pharmacologically relevant dose of ethanol, we simultaneously detect a) in the pVTA, a substance, 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), untraceable under control conditions, product of condensation between DA and ethanol’s first by-product, acetaldehyde; and b) in the AcbSh, a significant increase of DA release. Moreover, such newly generated salsolinol in the pVTA is responsible for increasing AcbSh DA release via μ opioid receptor (μOR) stimulation. In fact, inhibition of salsolinol’s generation in the pVTA or blockade of pVTA μORs prevents ethanol-increased ipsilateral, but not contralateral, AcbSh DA release. This evidence discloses the long-sought key mechanism of ethanol’s addictive potential and suggests the grounds for developing preventive and therapeutic strategies against abnormal consumption.

Abnormal consumption of ethanol, the ingredient responsible for alcoholic drinks’ addictive liability, causes millions of deaths yearly. Ethanol’s addictive potential is triggered through activation, by a still unknown mechanism, of the mesolimbic dopamine (DA) system, part of a key motivation circuit, DA neurons in the posterior ventral tegmental area (pVTA) projecting to the ipsilateral nucleus accumbens shell (AcbSh). The present in vivo brain microdialysis study, in dually-implanted rats with one probe in the pVTA and another in the ipsilateral or contralateral AcbSh, demonstrates this mechanism. As a consequence of the oral administration of a pharmacologically relevant dose of ethanol, we simultaneously detect a) in the pVTA, a substance, 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), untraceable under control conditions, product of condensation between DA and ethanol’s first by-product, acetaldehyde; and b) in the AcbSh, a significant increase of DA release. Moreover, such newly generated salsolinol in the pVTA is responsible for increasing AcbSh DA release via μ opioid receptor (μOR) stimulation. In fact, inhibition of salsolinol’s generation in the pVTA or blockade of pVTA μORs prevents ethanol-increased ipsilateral, but not contralateral, AcbSh DA release. This evidence discloses the long-sought key mechanism of ethanol’s addictive potential and suggests the grounds for developing preventive and therapeutic strategies against abnormal consumption.

Ethanol excites dopamine (DA) neurons in the posterior ventral tegmental area (pVTA). This effect is responsible for ethanol's motivational properties and may contribute to alcoholism. Evidence indicates that catalase-mediated conversion of ethanol into acetaldehyde in pVTA plays a critical role in this effect. Acetaldehyde, in the presence of DA, condensates with it to generate salsolinol. Salsolinol, when administered in pVTA, excites pVTA DA cells, elicits DA transmission in nucleus accumbens and sustains its self-administration in pVTA. Here we show, by using ex vivo electrophysiology, that ethanol and acetaldehyde, but not salsolinol, failed to stimulate pVTA DA cell activity in mice administered α-methyl-p-tyrosine, a DA biosynthesis inhibitor that reduces somatodendritic DA release. This effect was specific for ethanol and acetaldehyde since morphine, similarly to salsolinol, was able to excite pVTA DA cells in α-methyl-p-tyrosine-treated mice. However, when DA was bath applied in slices from α-methyl-p-tyrosine-treated mice, ethanol-induced excitation of pVTA DA neurons was restored. This effect requires ethanol oxidation into acetaldehyde given that, when H2 O2 -catalase system was impaired by either 3-amino-1,2,4-triazole or in vivo administration of α-lipoic acid, ethanol did not enhance DA cell activity. Finally, high performance liquid chromatography-tandem mass spectrometry analysis of bath medium detected salsolinol only after co-application of ethanol and DA in α-methyl-p-tyrosine-treated mice. These results demonstrate the relationship between ethanol and salsolinol effects on pVTA DA neurons, help to untangle the mechanism(s) of action of ethanol in this area and contribute to an exciting research avenue prosperous of theoretical and practical consequences.

Ethanol excites dopamine (DA) neurons in the posterior ventral tegmental area (pVTA). This effect is responsible for ethanol's motivational properties and may contribute to alcoholism. Evidence indicates that catalase-mediated conversion of ethanol into acetaldehyde in pVTA plays a critical role in this effect. Acetaldehyde, in the presence of DA, condensates with it to generate salsolinol. Salsolinol, when administered in pVTA, excites pVTA DA cells, elicits DA transmission in nucleus accumbens and sustains its self-administration in pVTA. Here we show, by using ex vivo electrophysiology, that ethanol and acetaldehyde, but not salsolinol, failed to stimulate pVTA DA cell activity in mice administered α-methyl-p-tyrosine, a DA biosynthesis inhibitor that reduces somatodendritic DA release. This effect was specific for ethanol and acetaldehyde since morphine, similarly to salsolinol, was able to excite pVTA DA cells in α-methyl-p-tyrosine-treated mice. However, when DA was bath applied in slices from α-methyl-p-tyrosine-treated mice, ethanol-induced excitation of pVTA DA neurons was restored. This effect requires ethanol oxidation into acetaldehyde given that, when H2 O2 -catalase system was impaired by either 3-amino-1,2,4-triazole or in vivo administration of α-lipoic acid, ethanol did not enhance DA cell activity. Finally, high performance liquid chromatography-tandem mass spectrometry analysis of bath medium detected salsolinol only after co-application of ethanol and DA in α-methyl-p-tyrosine-treated mice. These results demonstrate the relationship between ethanol and salsolinol effects on pVTA DA neurons, help to untangle the mechanism(s) of action of ethanol in this area and contribute to an exciting research avenue prosperous of theoretical and practical consequences.

Long-term spatial missions will require sustainable methods for biomass production using locally available resources. This study investigates the feasibility of cultivating Chlorella vulgaris, a high value microalgal specie, using a leachate of Martian regolith and synthetic human urine as nutrient sources. The microalga was grown in a standard medium (BBM) mixed with 0, 20, 40, 60, or 100 % Martian medium (MM). MM did not significantly affect final biomass concentrations. Total carbohydrate and protein contents decreased with increasing MM fractions between 0 % and 60 %, but biomass in the 100% MM showed the highest levels of carbohydrates and proteins (25.2 ± 0.9 % and 37.1 ± 1.4 % of the dry weight, respectively, against 19.0 ± 1.7 % and 32.0 ± 2.7 % in the absence of MM). In all MM-containing media, the fraction of the biomass represented by total lipids was lower (by 3.2 to 4.5%) when compared to BBM. Conversely, total carotenoids increased, with the highest value (97.3 ± 1.5 mg/100 g) measured with 20% MM. In a three-dimensional principal component analysis of triacylglycerols, samples clustered according to growth media; a strong impact of growth media on triacylglycerol profiles was observed. Overall, our findings suggest that microalgal biomass produced using regolith and urine can be used as a valuable component of astronauts' diet during missions to Mars.