Energy Deprivation Research Articles

Energy Poverty is Not Only a Matter of Income and Inequality. The Role of Socio-Political Factors for Alleviating Energy Needs in European Countries

The stringency of energy poverty in a country is usually related to low income and unequal distribution of earnings. In this paper, we enlarge the picture by showing how internal socio-political factors are associated with different measures of energy deprivation. Specifically, relying on the recently elaborated energy poverty indexes developed by OpenEXP, we show how energy deprivation among European countries correlates to a set of variables in which are included the governance indicators provided by the World Bank. Using different regression strategies, we find that the quality of institutions and regulatory processes are significantly related with the ability of European countries to effectively cope with energy poverty. On the side of policy, our empirical findings stress the importance and the potential effectiveness of targeted public interventions aimed at mitigating the impoverishment effects driven by fully deregulated energy markets.

Energy poverty: conceptualization and its link to exclusion. Brief review for Latin America

Abstract Energy is a critical input for any socioeconomic system and it has become a central point in sustainable development worldwide. Energy deprivation in its various degrees has given rise to the term Energy Poverty. The deprivations in access and quality of energy services sustained over time are elements that generate social exclusion processes and limit the development of the countries with these characteristics. The aim of this paper is to deepen the conceptual discussion of energy poverty and exclusion and the background regarding its measurement, as well as its link with the Just Energy Transition. Descriptive statistics are explored to assess the situation in the Latin American region. It is concluded that the limitations in access to basic energy services are significant, affecting more severely the population of countries with a low level of output and less socioeconomically favored.

Starvation-Sensitized and Oxygenation-Promoted Tumor Sonodynamic Therapy by a Cascade Enzymatic Approach.

The therapeutic outcomes of noninvasive sonodynamic therapy (SDT) are always compromised by tumor hypoxia, as well as inherent protective mechanisms of tumor. Herein, we report a simple cascade enzymatic approach of the concurrent glucose depletion and intratumoral oxygenation for starvation-sensitized and oxygenation-amplified sonodynamic therapy using a dual enzyme and sonosensitizer-loaded nanomedicine designated as GOD/CAT@ZPF-Lips. In particular, glucose oxidase- (GOD-) catalyzed glycolysis would cut off glucose supply within the tumor, resulting in the production of tumor hydrogen peroxide (H2O2) while causing tumor cells starvation. The generated H2O2 could subsequently be decomposed by catalase (CAT) to generate oxygen, which acts as reactants for the abundant singlet oxygen (1O2) production by loaded sonosensitizer hematoporphyrin monomethyl ether (HMME) upon the US irradiation, performing largely elevated therapeutic outcomes of SDT. In the meantime, the severe energy deprivation enabled by GOD-catalyzed glucose depletion would prevent tumor cells from executing protective mechanisms to defend themselves and make the tumor cells sensitized and succumbed to the cytotoxicity of 1O2. Eventually, GOD/CAT@ZPF-Lips demonstrate the excellent tumoral therapeutic effect of SDT in vivo without significant side effect through the cascade enzymatic starvation and oxygenation, and encouragingly, the tumor xenografts have been found completely eradicated in around 4 days by the intravenous injection of the nanomedicine without reoccurrence for as long as 20 days.

Impairment of AMPK-α2 augments detrusor contractions in bladder ischemia.

PurposeIschemia disrupts cellular energy homeostasis. Adenosine monophosphate-activated protein kinase alpha-2 (AMPK-α2) is a subunit of AMPK that senses cellular energy deprivation and signals metabolic stress. Our goal was to examine the expression levels and functional role of AMPK-α2 in bladder ischemia.Materials and MethodsIliac artery atherosclerosis and bladder ischemia were engendered in apolipoprotein E knockout rats by partial arterial endothelial denudation using a balloon catheter. After eight weeks, total and phosphorylated AMPK-α2 expression was analyzed by western blotting. Structural integrity of AMPK-α2 protein was assessed by Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS). Functional role of AMPK-α2 was examined by treating animals with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D ribofuranoside (AICAR). Tissue contractility was measured in the organ bath and bladder nerve density was examined by immunostaining.ResultsTotal AMPK-α2 expression increased in bladder ischemia, while phosphorylated AMPK-α2 was significantly downregulated. LC-MS/MS suggested post-translational modification of AMPK-α2 functional domains including phosphorylation sites, suggesting accumulation of catalytically inactive AMPK-α2 in bladder ischemia. Treatment of rats with AICAR diminished the force of overactive detrusor contractions and increased bladder capacity but did not have a significant effect on the frequency of bladder contractions. AICAR diminished contractile reactivity of ischemic tissues in the organ bath and prevented loss of nerve fibers in bladder ischemia.ConclusionsIschemia induces post-translational modification of AMPK-α2 protein. Impairment of AMPK-α2 may contribute to overactive detrusor contractions and loss of nerve fibers in bladder ischemia. AMPK activators may have therapeutic potential against detrusor overactivity and neurodegeneration in bladder conditions involving ischemia.

New Dimensions of Vulnerability to Energy and Transport Poverty

As we decarbonise societies, we need to consider how such transitions interconnect energy and transport systems. In this Commentary, we argue that we need a better understanding of who may be vulnerable in low-carbon transitions. Current energy poverty definitions and metrics focus overwhelmingly on energy service consumption within the home, yet similar issues in the transport sector are often neglected. Failure to account for the intersections between energy and transport poverty may deepen structural forms of deprivation and worsen social and material inequalities, therefore preventing equitable transitions.

The Motivation for Incorporation of Microgrid Technology in Rooftop Solar Photovoltaic Deployment to Enhance Energy Economics

Deployment of rooftop solar Photovoltaic technology in domestic premises plays a significant role in accomplishing renewable energy transformation. The majority of domestic consumers still do not have a positive perception about adopting rooftop solar PV technology, due to its high capital cost and prolonged payback period. In this aspect, the proposed work identifies the factors causing energy deprivation in the present distribution and utilization system. To explicitly express the importance of the present work, an extensive case study based on an Indian scenario has been carried out to investigate where the losses occur in the existing distribution system and how the solar power and its storage system have been ineffectively utilized. The deep investigation has thrown light on several issues that lead to the performance deterioration of PV technology. Finally, in this work, a scheme to incorporate hybrid microgrid technology in the domestic distribution network has been proposed to effectively manage the distribution system and to efficiently utilize solar power and its storage systems. The real-time electricity tariff data have been taken for cost comparison and payback period calculations to prove the effectiveness of the proposed method. Crucial comparisons have been presented based on energy saving and carbon dioxide CO2 emission reduction strategies.

Variability of mitochondrial energy balance across brain regions.

Brain is not homogenous and neurons from various brain regions are known to have different vulnerabilities to mitochondrial mutations and mitochondrial toxins. However, it is not clear if this vulnerability is connected to different energy metabolism in specific brain regions. Here, using live-cell imaging, we compared mitochondrial membrane potential and nicotinamide adenine dinucleotide (NADH) redox balance in acute rat brain slices in different brain regions and further detailed the mitochondrial metabolism in primary neurons and astrocytes from rat cortex, midbrain and cerebellum. We have found that mitochondrial membrane potential is higher in brain slices from the hippocampus and brain stem. In primary co-cultures, mitochondrial membrane potential in astrocytes was lower than in neurons, whereas in midbrain cells it was higher than in cortex and cerebellum. The rate of NADH production and mitochondrial NADH pool were highest in acute slices from midbrain and midbrain primary neurons and astrocytes. Although the level of adenosine tri phosphate (ATP) was similar among primary neurons and astrocytes from cortex, midbrain and cerebellum, the rate of ATP consumption was highest in midbrain cells that lead to faster neuronal and astrocytic collapse in response to inhibitors of ATP production. Thus, midbrain neurons and astrocytes have a higher metabolic rate and ATP consumption that makes them more vulnerable to energy deprivation.

CORRECTION: ABI1 and PP2CA phosphatases are negative regulators of Snf1-related protein kinase1 signaling in Arabidopsis.

Plant survival under environmental stress requires the integration of multiple signaling pathways into a coordinated response, but the molecular mechanisms underlying this integration are poorly understood. Stress-derived energy deprivation activates the Snf1-related protein kinases1 (SnRK1s), triggering a vast transcriptional and metabolic reprogramming that restores homeostasis and promotes tolerance to adverse conditions. Here, we show that two clade A type 2C protein phosphatases (PP2Cs), established repressors of the abscisic acid (ABA) hormonal pathway, interact with the SnRK1 catalytic subunit causing its dephosphorylation and inactivation. Accordingly, SnRK1 repression is abrogated in double and quadruple pp2c knockout mutants, provoking, similarly to SnRK1 overexpression, sugar hypersensitivity during early seedling development. Reporter gene assays and SnRK1 target gene expression analyses further demonstrate that PP2C inhibition by ABA results in SnRK1 activation, promoting SnRK1 signaling during stress and once the energy deficit subsides. Consistent with this, SnRK1 and ABA induce largely overlapping transcriptional responses. Hence, the PP2C hub allows the coordinated activation of ABA and energy signaling, strengthening the stress response through the cooperation of two key and complementary pathways.

Counting the cost: Coping with tariff increases amidst power supply shortfalls in urban households in Ethiopia

Although affordability is important, people do not need to be money poor to experience energy deprivation. This paper examines how an electricity tariff increase affects household energy consumption by situating the price change within the broader context of energy service provision in Ethiopia. We place households’ lived experience in interaction with the institutional and infrastructural dynamics that constitute the energy sector in Addis Ababa to observe how the price increase intersects with service provision. Since the tariff increase was implemented, households have changed their daily routines to control cost. Our findings show that energy consumption behaviour is also shaped by service-related inadequacies (unreliable supply and frequent power outages). However, families coping capacity (to the tariff increase and power supply shortfalls) is undermined by an energy market that is rife with information asymmetries and uncertainties. Thus, although socioeconomic factors underpin the energy insecurity households experience, inadequate supply, and diminishing confidence in service providing institutions appears to heighten their vulnerability. The paper argues that while the price change has an overall effect on consumption, its impact needs to be seen within the context of its systemic interaction with the broader energy governance and service delivery challenges.

Recent Advances in the Pathophysiology of Fatty Acid Oxidation Defects: Secondary Alterations of Bioenergetics and Mitochondrial Calcium Homeostasis Caused by the Accumulating Fatty Acids.

Deficiencies of medium-chain acyl-CoA dehydrogenase, mitochondrial trifunctional protein, isolated long-chain 3-hydroxyacyl-CoA dehydrogenase, and very long-chain acyl-CoA dehydrogenase activities are considered the most frequent fatty acid oxidation defects (FAOD). They are biochemically characterized by the accumulation of medium-chain, long-chain hydroxyl, and long-chain fatty acids and derivatives, respectively, in tissues and biological fluids of the affected patients. Clinical manifestations commonly include hypoglycemia, cardiomyopathy, and recurrent rhabdomyolysis. Although the pathogenesis of these diseases is still poorly understood, energy deprivation secondary to blockage of fatty acid degradation seems to play an important role. However, recent evidence indicates that the predominant fatty acids accumulating in these disorders disrupt mitochondrial functions and are involved in their pathophysiology, possibly explaining the lactic acidosis, mitochondrial morphological alterations, and altered mitochondrial biochemical parameters found in tissues and cultured fibroblasts from some affected patients and also in animal models of these diseases. In this review, we will update the present knowledge on disturbances of mitochondrial bioenergetics, calcium homeostasis, uncoupling of oxidative phosphorylation, and mitochondrial permeability transition induction provoked by the major fatty acids accumulating in prevalent FAOD. It is emphasized that further in vivo studies carried out in tissues from affected patients and from animal genetic models of these disorders are necessary to confirm the present evidence mostly achieved from in vitro experiments.

Hydrogen-Oxidizing Bacteria Are Abundant in Desert Soils and Strongly Stimulated by Hydration.

How the diverse bacterial communities inhabiting desert soils maintain energy and carbon needs is much debated. Traditionally, most bacteria are thought to persist by using organic carbon synthesized by photoautotrophs following transient hydration events. Recent studies focused on Antarctic desert soils have revealed, however, that some bacteria use atmospheric trace gases, such as hydrogen (H2), to conserve energy and fix carbon independently of photosynthesis. In this study, we investigated whether atmospheric H2 oxidation occurs in four nonpolar desert soils and compared this process to photosynthesis. To do so, we first profiled the distribution, expression, and activities of hydrogenases and photosystems in surface soils collected from the South Australian desert over a simulated hydration-desiccation cycle. Hydrogenase-encoding sequences were abundant in the metagenomes and metatranscriptomes and were detected in actinobacterial, acidobacterial, and cyanobacterial metagenome-assembled genomes. Native dry soil samples mediated H2 oxidation, but rates increased 950-fold following wetting. Oxygenic and anoxygenic phototrophs were also detected in the community but at lower abundances. Hydration significantly stimulated rates of photosynthetic carbon fixation and, to a lesser extent, dark carbon assimilation. Hydrogenase genes were also widespread in samples from three other climatically distinct deserts, the Namib, Gobi, and Mojave, and atmospheric H2 oxidation was also greatly stimulated by hydration at these sites. Together, these findings highlight that H2 is an important, hitherto-overlooked energy source supporting bacterial communities in desert soils. Contrary to our previous hypotheses, however, H2 oxidation occurs simultaneously rather than alternately with photosynthesis in such ecosystems and may even be mediated by some photoautotrophs.IMPORTANCE Desert ecosystems, spanning a third of the earth's surface, harbor remarkably diverse microbial life despite having a low potential for photosynthesis. In this work, we reveal that atmospheric hydrogen serves as a major previously overlooked energy source for a large proportion of desert bacteria. We show that both chemoheterotrophic and photoautotrophic bacteria have the potential to oxidize hydrogen across deserts sampled across four continents. Whereas hydrogen oxidation was slow in native dry deserts, it increased by three orders of magnitude together with photosynthesis following hydration. This study revealed that continual harvesting of atmospheric energy sources may be a major way that desert communities adapt to long periods of water and energy deprivation, with significant ecological and biogeochemical ramifications.

Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia.

In several neurodegenerative disorders, axonal pathology may originate from impaired oligodendrocyte-to-axon support of energy substrates. We previously established transgenic mice that allow measuring axonal ATP levels in electrically active optic nerves. Here, we utilize this technique to explore axonal ATP dynamics in the Plpnull/y mouse model of spastic paraplegia. Optic nerves from Plpnull/y mice exhibited lower and more variable basal axonal ATP levels and reduced compound action potential (CAP) amplitudes, providing a missing link between axonal pathology and a role of oligodendrocytes in brain energy metabolism. Surprisingly, when Plpnull/y optic nerves are challenged with transient glucose deprivation, both ATP levels and CAP decline slower, but recover faster upon reperfusion of glucose. Structurally, myelin sheaths display an increased frequency of cytosolic channels comprising glucose and monocarboxylate transporters, possibly facilitating accessibility of energy substrates to the axon. These data imply that complex metabolic alterations of the axon–myelin unit contribute to the phenotype of Plpnull/y mice.

Measuring fuel poverty in tropical territories: A latent class model

There are well established strategies for measuring fuel poverty in developed countries based on heating factors correlated with household income (expenditure, heating restriction or cold houses), but they do not translate well to tropical regions where climatic conditions and socioeconomic contexts entail different energy use. Fuel poverty in tropical regions has never been defined. We propose a new framework for the identification of fuel-poor households based on Sen's capability approach. We employ latent class model (LCM) methodology to accurately assess fuel poverty in tropical areas using observable objective characteristics of decent, safe and healthy dwellings. This approach enables us to categorize households as fuel-poor or fuel-sufficient. It is also possible to extend the model further by considering the multi-dimensional phenomenon of fuel poverty. We find that the most deprived represent approximately 12% of the population, while 32% of the population is expected to belong to the fuel-sufficient class. An intermediate class encompassing 56% of the population represents vulnerable households that could easily be affected by an exogenous shock. Energy deprivation is much more complex and multidimensional than a binary phenomenon, implying that fuel poverty can be measured with different degrees of exposure. With this research, we enable policy makers to identify a target group of households that should be a top priority in fighting fuel poverty in tropical regions.

Repurposing disulfiram to induce OSCC cell death by cristae dysfunction promoted autophagy

Disulfiram has been repurposed as a potential candidate to suppress various cancers. However, its anti-tumor effects and molecular mechanisms of oral squamous cell carcinoma remain unclear. In this study, we aimed to assess the anti-cancer activity and underlying mechanisms of disulfiram in the context of oral squamous cell carcinoma. We tested the cytotoxicity of disulfiram in oral squamous cell carcinoma using a 3D culture model and a PDX model. Cell proliferation, cell death, and related signaling pathways were evaluated. Mitochondrial DNA copy number, mitochondrial respiration, mitochondrial mass, and mitochondrial complexes were analyzed. Disulfiram can induce excessive autophagy in oral squamous cell carcinoma cells as a result of OXPHOS deficiency. Disulfiram-induced OPA1 degradation can impair the functional cristae structure, which results in a dramatic reduction in mitochondrial respiration capability as well as ATP production. Subsequently, energy deprivation leads to excessive autophagy through AMPK activation. In addition, exogenous ATP blocked the activation of AMPK and rescued disulfiram-induced cell death. DSF targets mitochondrial inner membrane protein OPA1 to disturb the energy supply, triggering excessive autophagy, and cell death in OSCC. Our study suggests OPA1-dependent ATP generation is pharmacologically targetable in OSCC treatment.

Male-biased fasting-induced changes inhepatic tauro-cholic acid and plasma cholesterolin Sult2a8-haplodeficient mice.

SULT2A8 is a male-predominant and liver-specific mouse cytosolic sulfotransferase (SULT) that sulfonates 7α-hydroxyl (7α-OH) bile acids in vitro. Sulfonation regulates bile acid homeostasis, which in turn regulates cholesterol and energy metabolism. Using the Sult2a8-heterozygous (HT) mouse model created earlier in our laboratory, we aimed to investigate the physiological role of SULT2A8 in sulfonating 7α-OH bile acids and its impact on energy metabolism in vivo under both fed and energy-deprivation conditions. Disruption of one allele of the Sult2a8 gene in male HT mice resulted in losing ~ 50% of the 7α-OH sulfonating activity compared to wild-type (WT) control, but no significant change in female HT mice. Under the fed condition comparing the levels of hepatic and biliary bile acids as well as plasma/serum energy metabolites, HT mice displayed a profile similar to that of WT mice, suggesting that the Sult2a8-haplodeficient mice conducted normal energy metabolism. However, after 48-h fasting, a significant decrease in plasma cholesterol level was found in male HT mice but without any significant reduction in female HT mice. Of interest, in male Sult2a8-haplodeficient mice, an increase of the hepatic taurine-conjugated cholic acid level was noted but no noticeable change in other tested bile acids after fasting. Taken together, SULT2A8 is a male-specific and key hepatic SULT in metabolizing 7α-OH primary bile acids. During energy deprivation, SULT2A8 is required to maintain the bile acid and cholesterol metabolism, suggesting SULT is a potential therapeutic target for controlling metabolic diseases.

Sex differences in the effect of acute fasting on excitatory and inhibitory synapses onto ventral tegmental area dopamine neurons.

Fasting can increase motivation for food and can energize reward-seeking. Ventral tegmental area (VTA) dopamine neurons respond to motivationally relevant information and fasting can influence mesolimbic dopamine concentration. An acute overnight fast differentially alters food approach behaviours and excitatory synaptic transmission onto VTA dopamine neurons of male or female mice. While inhibitory synapses onto VTA dopamine neurons are not altered by fasting in male or female mice, male mice had strengthened excitatory synapses whereas female mice had increased endocannabinoid-mediated short-term plasticity at excitatory synapses. These results help us understand how fasting differentially influences excitatory synaptic transmission onto dopamine neurons and may inform different strategies for fasting-induced food seeking by male and female mice. Dopamine neurons in the ventral tegmental area (VTA) are important for energizing goal-directed behaviour towards food and are sensitive to changes in metabolic states. Fasting increases the incentive motivation for food and the mobilization of energy stores and has sex-dependent effects. However, it is unknown how acute fasting alters excitatory or inhibitory synaptic transmission onto VTA dopamine neurons. An acute 16h overnight fast induced increased food-seeking behaviour that was more predominant in male mice. Fasting increased miniature excitatory postsynaptic current frequency and amplitude in male, but not female, mice. This effect was not due to altered release probability as there was no change in the paired pulse ratio, nor was it due to an altered postsynaptic response as there was no change in the AMPA receptor/NMDA receptor ratio or response to glutamate uncaging. However, this effect was consistent with an increase in the number of release sites. In addition, depolarization-induced suppression of excitation, a measure of short-term endocannabinoid-mediated plasticity, was enhanced in female but not male fasted mice. There were no fasting-induced changes at inhibitory synapses onto dopamine neurons of male or female mice. Taken together, these results demonstrate that fasting influences excitatory synapses differentially in male and female mice, but preserves inhibitory synapses onto dopamine neurons, indicating that the mesolimbic circuits of male and female mice respond differently to acute energy deprivation.

Glycolytic inhibition by resveratrol prevents myoblast cell death caused by glucose deprivation and hypoxia; a possible application to the three-dimensional tissue construction

Decreased cell viability resulting from a severe condition of nutrients deprivation and hypoxia has been the major obstacle in three-dimensional (3D) tissue construction. Therefore, technical improvement which prevents cell death caused by starvation and low oxygen is desired for the development of large, thick tissues. We focused on the anti-glycolytic effect of resveratrol (RSV), a naturally-occurring polyphenol known as a caloric restriction mimetic, and investigated its cytoprotective effect in two-dimensional (2D) and 3D-cell culture using H9c2 rat myoblast cells. Glucose deprivation by culturing with low glucose media caused time- and dose-dependent cell death in H9c2 cells. In contrast, RSV treatment at 100μM significantly increased the cell viability by preventing cell death. RSV showed anti-glycolytic effect associated with a down-regulation of glycolytic genes (GLUT1, PKM2) and glucose uptake activity, and increased the activation of AMP-activated protein kinase (AMPK), an essential cellular energy sensor activated in the condition of energy deprivation. RSV treatment markedly improved the viability of myoblast cells cultured in a hypoxic, low glucose condition and attenuated the up-regulation of glycolytic genes by hypoxic response. In 3D-cultured model, spheroids constructed with RSV-treated cells showed improved cell viability and intact histological appearance compared with control. These results suggest that glycolytic inhibition by RSV decreases the glucose usage of myoblast cells, therefore, prevents cell death caused by nutrient deprivation and hypoxic condition. Our finding provides useful information to improve cell viability in a condition that nutrients and oxygen are low in supply, and be a possible application to the 3D-tissue construction.

Apomorphine induces mitochondrial-dysfunction-dependent apoptosis in choriocarcinoma.

Apomorphine is a derivative of morphine that is used for the treatment of Parkinson's disease because of its effects on the hypothalamus. Therapeutic effects of apomorphine have also been reported for various neurological diseases and cancers. However, the molecular mechanisms of the antitumor effects of apomorphine are not clear, especially with respect to choriocarcinoma. This is the first study to elucidate the anticancer effects of apomorphine on choriocarcinoma. We found that apomorphine suppressed the viability, proliferation, ATP production, and spheroid formation of JEG3 and JAR choriocarcinoma cells. Moreover, apomorphine activated the intrinsic apoptosis pathway by activating caspases and inhibited the production of anti-apoptotic proteins in choriocarcinoma cells. Further, apomorphine caused depolarization of mitochondria, calcium overload, energy deprivation, and endoplasmic reticulum stress in JEG3 and JAR cells. We confirmed synergistic effects of apomorphine with paclitaxel, a traditional chemotherapeutic agent, and propose that apomorphine could be a potential therapeutic agent in choriocarcinoma and an important candidate for drug repositioning that could help overcome resistance to conventional chemotherapy.

Multidimensional Energy Poverty and Mental Health: Micro-Level Evidence from Ghana.

Regardless of growing interest and awareness of the effect of energy poverty on mental health, studies on this linkage have mainly relied on unidimensional measures of energy poverty with much concentration on advanced economies. Employing a two-wave socioeconomic survey, we analyzed the impact of multidimensional energy poverty on mental health in Ghana. We found energy poverty to heighten the chances of being mentally unhealthy. Using prices of liquefied petroleum gas and electricity as instruments for multidimensional energy poverty, we found that a rise in energy deprivation is associated with a 0.562-, 1.494- and 1.867-fold increase in the odds of being mildly, moderately and severely depressed, respectively. Among the indicators of multidimensional energy poverty, a deprivation in household appliance ownership (refrigerator ownership), recorded the highest impact on the depression levels of household heads. We concluded by urging policymakers to adopt a holistic approach in solving issues of energy poverty where simultaneous attention is given to all the dimensions of energy poverty since they collectively have detrimental effects on mental health, especially in a developing country setting.

Effect of energy deprivation on metabolite release by anaerobic marine naphthalene-degrading sulfate-reducing bacteria.

The aromatic hydrocarbon naphthalene, which occurs in coal and oil, can be degraded by aerobic or anaerobic microorganisms. A wide-spread electron acceptor for the latter is sulfate. Evidence for in situ naphthalene degradation stems in particular from the detection of 2-naphthoate and [5,6,7,8]-tetrahydro-2-naphthoate in oil field samples. Because such intermediates are usually not detected in laboratory cultures with high sulfate concentrations, one may suppose that conditions in reservoirs, such as sulfate limitation, trigger metabolite release. Indeed, if naphthalene-grown cells of marine sulfate-reducing Deltaproteobacteria (strains NaphS2, NaphS3 and NaphS6) were transferred to sulfate-free medium, they released 2-naphthoate and [5,6,7,8]-tetrahydro-2-naphthoate while still consuming naphthalene. With 2-naphthoate as initial substrate, cells produced [5,6,7,8]-tetrahydro-2-naphthoate and the hydrocarbon, naphthalene, indicating reversibility of the initial naphthalene-metabolizing reaction. The reactions in the absence of sulfate were not coupled to observable growth. Excretion of naphthalene-derived metabolites was also achieved in sulfate-rich medium upon addition of the protonophore carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone or the ATPase inhibitor N,N'-dicyclohexylcarbodiimide. In conclusion, obstruction of electron flow and energy gain by sulfate limitation offers an explanation for the occurrence of naphthalene-derived metabolites in oil reservoirs, and provides a simple experimental tool for gaining insights into the anaerobic naphthalene oxidation pathway from an energetic perspective.