Snow-Dependent Biogeochemical Cycling of Polycyclic Aromatic Hydrocarbons at Coastal Antarctica.

The temporal trend of polycyclic aromatic hydrocarbons (PAHs) in coastal waters with highly dynamic sources and sinks is largely unknown, especially for polar regions. Here, we show the concurrent measurements of 73 individual PAHs and environmental data, including the composition of the bacterial community, during three austral summers at coastal Livingston (2015 and 2018) and Deception (2017) islands (Antarctica). The Livingston 2015 campaign was characterized by a larger snow melting input of PAHs and nutrients. The assessment of PAH diagnostic ratios, such as parent to alkyl-PAHs or LMW to HMW PAHs, showed that there was a larger biodegradation during the Livingston 2015 campaign than in the Deception 2017 and Livingston 2018 campaigns. The biogeochemical cycling, including microbial degradation, was thus yearly dependent on snow-derived inputs of matter, including PAHs, consistent with the microbial community significantly different between the different campaigns. The bivariate correlations between bacterial taxa and PAH concentrations showed that a decrease in PAH concentrations was concurrent with the higher abundance of some bacterial taxa, specifically the order Pseudomonadales in the class Gammaproteobacteria, known facultative hydrocarbonoclastic bacteria previously reported in degradation studies of oil spills. The work shows the potential for elucidation of biogeochemical processes by intensive field-derived time series, even in the harsh and highly variable Antarctic environment.

Bacterial responses to background organic pollutants in the northeast subarctic Pacific Ocean.

Thousands of man-made synthetic chemicals are released to oceans and compose the anthropogenic dissolved organic carbon (ADOC). Little is known about the effects of this chronic pollution on marine microbiome activities. In this study, we measured the pollution level at three sites in the Northeast Subarctic Pacific Ocean (NESAP) and investigated how mixtures of three model families of ADOC at different environmentally relevant concentrations affected naturally occurring marine bacterioplankton communities' structure and metabolic functioning. The offshore northernmost site (North) had the lowest concentrations of hydrocarbons, as well as organophosphate ester plasticizers, contrasting with the two other continental shelf sites, the southern coastal site (South) being the most contaminated. At North, ADOC stimulated bacterial growth and promoted an increase in the contribution of some Gammaproteobacteria groups (e.g. Alteromonadales) to the 16 rRNA pool. These groups are described as fast responders after oil spills. In contrast, minor changes in South microbiome activities were observed. Gene expression profiles at Central showed the coexistence of ADOC degradation and stress-response strategies to cope with ADOC toxicities. These results show that marine microbial communities at three distinct domains in NESAP are influenced by background concentrations of ADOC, expanding previous assessments for polar and temperate waters.

Rain Amplification of Persistent Organic Pollutants.

Scavenging of gas- and aerosol-phase organic pollutants by rain is an efficient wet deposition mechanism of organic pollutants. However, whereas snow has been identified as a key amplification mechanism of fugacities in cold environments, rain has received less attention in terms of amplification of organic pollutants. In this work, we provide new measurements of concentrations of perfluoroalkyl substances (PFAS), organophosphate esters (OPEs), and polycyclic aromatic hydrocarbons (PAHs) in rain from Antarctica, showing high scavenging ratios. Furthermore, a meta-analysis of previously published concentrations in air and rain was performed, with 46 works covering different climatic regions and a wide range of chemical classes, including PFAS, OPEs, PAHs, polychlorinated biphenyls and organochlorine compounds, polybromodiphenyl ethers, and dioxins. The rain-aerosol (KRP) and rain-gas (KRG) partition constants averaged 105.5 and 104.1, respectively, but showed large variability. The high field-derived values of KRG are consistent with adsorption onto the raindrops as a scavenging mechanism, in addition to gas-water absorption. The amplification of fugacities by rain deposition was up to 3 orders of magnitude for all chemical classes and was comparable to that due to snow. The amplification of concentrations and fugacities by rain underscores its relevance, explaining the occurrence of organic pollutants in environments across different climatic regions.

Differential effects of AMP-activated protein kinase in isolated rat atria subjected to simulated ischemia-reperfusion depending on the energetic substrates available.

AMP-activated protein kinase (AMPK) is a serine-threonine kinase that functions primarily as a metabolic sensor to coordinate anabolic and catabolic processes in the cell, via phosphorylation of multiple proteins involved in metabolic pathways, aimed to re-establish energy homeostasis at a cell-autonomous level. Myocardial ischemia and reperfusion represents a metabolic stress situation for myocytes. Whether AMPK plays a critical role in the metabolic and functional responses involved in these conditions remains uncertain. In this study, in order to gain a deeper insight into the role of endogenous AMPK activation during myocardial ischemia and reperfusion, we explored the effects of the pharmacological inhibition of AMPK on contractile function rat, contractile reserve, tissue lactate production, tissue ATP content, and cellular viability. For this aim, isolated atria subjected to simulated 75 min ischemia-75 min reperfusion (Is-Rs) in the presence or absence of the pharmacological inhibitor of AMPK (compound C) were used. Since in most clinical situations of ischemia-reperfusion the heart is exposed to high levels of fatty acids, the influence of palmitate present in the incubation medium was also investigated. The present results suggest that AMPK activity significantly increases during Is, remaining activated during Rs. The results support that intrinsic activation of AMPK has functional protective effects in the reperfused atria when glucose is the only available energetic substrate whereas it is deleterious when palmitate is also available. Cellular viability was not affected by either of these conditions.

Effects of 3-methyladenine on isolated left atria subjected to simulated ischaemia-reperfusion.

Although autophagy is a prominent feature of myocardial ischaemia and reperfusion, its functional significance is unclear and controversial. In order to gain a deeper insight into the role of autophagy in myocardial ischaemia-reperfusion, we explored the effects of the pharmacological inhibitor of autophagy 3-methyladenine (3-MA). Isolated rat atria subjected to simulated 75-min ischaemia/75-min reperfusion (Is-Rs) in the presence or absence of 3-MA were used. The LC3-II/LC3-I ratio, an indicator of autophagosome formation, did not increase after ischaemia either in the presence or absence of 3-MA, but there was significant enhancement during reperfusion, which was prevented by the presence of 3-MA. The autophagy inhibitor also increased p62 protein, one of the specific substrates degraded through the autophagy-lysosomal pathway. Electron micrographs showed double membrane autophagosome-like structures during reperfusion, which were absent in atria subjected to Is-Rs in the presence of 3-MA. These findings suggest that this agent inhibited the autophagic flux under the present experimental conditions. Inhibition of autophagy during Is-Rs was accompanied by a high incidence of tachyarrhythmias during reperfusion, and a decrease in the maximal inotropic response to ß-adrenergic and to calcium stimulation at the end of Is-Rs. Deterioration of mitochondrial morphology and function, without affecting cell viability, was observed in atria subjected to Is-Rs in the presence of 3-MA. The present results suggest an association between the inhibition of autophagy and functional alterations of the cells that have undergone sublethal stress, and have been able to recover in this experimental model of ischaemia-reperfusion.

Metatranscriptomic responses and microbial degradation of background polycyclic aromatic hydrocarbons in the coastal Mediterranean and Antarctica.

Although microbial degradation is a key sink of polycyclic aromatic hydrocarbons (PAH) in surface seawaters, there is a dearth of field-based evidences of regional divergences in biodegradation and the effects of PAHs on site-specific microbial communities. We compared the magnitude of PAH degradation and its impacts in short-term incubations of coastal Mediterranean and the Maritime Antarctica microbiomes with environmentally relevant concentrations of PAHs. Mediterranean bacteria readily degraded the less hydrophobic PAHs, with rates averaging 4.72 ± 0.5 ng L h-1. Metatranscriptomic responses showed significant enrichments of genes associated to horizontal gene transfer, stress response, and PAH degradation, mainly harbored by Alphaproteobacteria. Community composition changed and increased relative abundances of Bacteroidota and Flavobacteriales. In Antarctic waters, there was no degradation of PAH, and minimal metatranscriptome responses were observed. These results provide evidence for factors such as geographic region, community composition, and pre-exposure history to predict PAH biodegradation in seawater.

Inputs, amplification and sinks of perfluoroalkyl substances at coastal Antarctica.

The sources, biogeochemical controls and sinks of perfluoroalkyl substances, such as perfluoroalkyl acids (PFAAs), in polar coastal regions are largely unknown. These were evaluated by measuring a large multi-compartment dataset of PFAAs concentrations at coastal Livingston and Deception Islands (maritime Antarctica) during three austral summers. PFAAs were abundant in atmospheric-derived samples (aerosols, rain, snow), consistent with the importance of atmospheric deposition as an input of PFAAs to Antarctica. Such PFAAs deposition was unequivocally demonstrated by the occurrence of PFAAs in small Antarctic lakes. Several lines of evidence supported the relevant amplification of PFAAs concentrations in surface waters driven by snow scavenging of sea-spray aerosol-bound PFAAs followed by snow-melting. For example, vertical profiles showed higher PFAAs concentrations at lower-salinity surface seawaters, and PFAAs concentrations in snow were significantly higher than in seawater. The higher levels of PFAAs at Deception Island than at Livingston Island are consistent with the semi-enclosed nature of the bay. Concentrations of PFOS decreased from 2014 to 2018, consistent with observations in other oceans. The sink of PFAAs due to the biological pump, transfer to the food web, and losses due to sea-spray aerosols alone are unlikely to have driven the decrease in PFOS concentrations. An exploratory assessment of the potential sinks of PFAAs suggests that microbial degradation of perfluoroalkyl sulfonates should be a research priority for the evaluation of PFAAs persistence in the coming decade.

Polycyclic Aromatic Hydrocarbon Degradation in the Sea-Surface Microlayer at Coastal Antarctica.

As much as 400 Tg of carbon from airborne semivolatile aromatic hydrocarbons is deposited to the oceans every year, the largest identified source of anthropogenic organic carbon to the ocean. Microbial degradation is a key sink of these pollutants in surface waters, but has received little attention in polar environments. We have challenged Antarctic microbial communities from the sea-surface microlayer (SML) and the subsurface layer (SSL) with polycyclic aromatic hydrocarbons (PAHs) at environmentally relevant concentrations. PAH degradation rates and the microbial responses at both taxonomical and functional levels were assessed. Evidence for faster removal rates was observed in the SML, with rates 2.6-fold higher than in the SSL. In the SML, the highest removal rates were observed for the more hydrophobic and particle-bound PAHs. After 24 h of PAHs exposure, particle-associated bacteria in the SML showed the highest number of significant changes in their composition. These included significant enrichments of several hydrocarbonoclastic bacteria, especially the fast-growing genera Pseudoalteromonas, which increased their relative abundances by eightfold. Simultaneous metatranscriptomic analysis showed that the free-living fraction of SML was the most active fraction, especially for members of the order Alteromonadales, which includes Pseudoalteromonas. Their key role in PAHs biodegradation in polar environments should be elucidated in further studies. This study highlights the relevant role of bacterial populations inhabiting the sea-surface microlayer, especially the particle-associated habitat, as relevant bioreactors for the removal of aromatic hydrocarbons in the oceans.

Restricted feeding improves postischemic recovery of Langendorff-perfused rat hearts.

The goal of the present study was to assess the effects of a restricted feeding schedule (RFS) on postischemic contractile recovery in relation to triacylglycerol (TAG), glycogen, and ATP content. Glucose-6-phosphate dehydrogenase (G6PDH) activity, reduced/oxidized glutathione ratio (GSH/GSSG), and thiobarbituric acid reactive substances (TBARS) levels were also determined. Isolated rat hearts entrained to daily RFS (2 h food access starting at 1200) or fed ad libitum (FED) for 3 weeks were Langendorff-perfused (25 min ischemia, 30 min reperfusion) with Krebs-Ringer bicarbonate solution (10 mmol/L glucose). RFS improved the recovery of contractility and reduced creatine kinase (CK) release upon reperfusion. Further, at the end of reperfusion, RFS hearts exhibited increased G6PDH activity and repletion of tissue glycogen, TAG, and ATP that was not observed in the FED hearts. GSH/GSSG at the end of reperfusion fell to the same value in both nutritional states, and TBARS levels were higher in the RFS hearts. In conclusion, RFS improved postischemic functional recovery, which was accompanied by a reduction in CK release and a striking energy recovery. Although enhanced G6PDH activity was displayed, RFS was unable to reduce lipid peroxidation, supporting a clear dissociation between protection against mechanical dysfunction and CK release on the one hand and oxidative damage on the other.

Large Enrichment of Anthropogenic Organic Matter Degrading Bacteria in the Sea-Surface Microlayer at Coastal Livingston Island (Antarctica).

The composition of bacteria inhabiting the sea-surface microlayer (SML) is poorly characterized globally and yet undescribed for the Southern Ocean, despite their relevance for the biogeochemistry of the surface ocean. We report the abundances and diversity of bacteria inhabiting the SML and the subsurface waters (SSL) determined from a unique sample set from a polar coastal ecosystem (Livingston Island, Antarctica). From early to late austral summer (January-March 2018), we consistently found a higher abundance of bacteria in the SML than in the SSL. The SML was enriched in some Gammaproteobacteria genus such as Pseudoalteromonas, Pseudomonas, and Colwellia, known to degrade a wide range of semivolatile, hydrophobic, and surfactant-like organic pollutants. Hydrocarbons and other synthetic chemicals including surfactants, such as perfluoroalkyl substances (PFAS), reach remote marine environments by atmospheric transport and deposition and by oceanic currents, and are known to accumulate in the SML. Relative abundances of specific SML-enriched bacterial groups were significantly correlated to concentrations of PFASs, taken as a proxy of hydrophobic anthropogenic pollutants present in the SML and its stability. Our observations provide evidence for an important pollutant-bacteria interaction in the marine SML. Given that pollutant emissions have increased during the Anthropocene, our results point to the need to assess chemical pollution as a factor modulating marine microbiomes in the contemporaneous and future oceans.

Anthropogenic dissolved organic carbon and marine microbiomes.

Thousands of synthetic chemicals and hydrocarbons are released to the marine environment composing the anthropogenic dissolved organic carbon (ADOC). Most ADOC is disproportionally hydrophobic, and consequently, its concentrations in the cell membranes are between a thousand and hundred million fold higher than those in the dissolved phase. Marine microorganisms respond to ADOC by multiple strategies ranging from ADOC degradation to detoxifying metabolisms. We argue that the increasing concentrations of ADOC in the oceans deriving from rivers, atmospheric deposition, and plastic leachates can have an effect on the health of the oceans and influence the major biogeochemical cycles, thus influencing the Earth system during the Anthropocene.

Enrichment of perfluoroalkyl substances in the sea-surface microlayer and sea-spray aerosols in the Southern Ocean.

Sea-spray (or sea-salt) aerosol (SSA) formation and their subsequent atmospheric transport and deposition have been suggested to play a prominent role in the occurrence of ionizable perfluoroalkyl substances (PFAS) in the maritime Antarctica and other remote regions. However, field studies on SSA's role as vector of transport of PFAS are lacking. Following a multiphase approach, seawater (SW), the sea-surface microlayer (SML) and SSA were sampled simultaneously at South Bay (Livingston Island, Antarctica). Average PFAS concentrations were 313 pg L-1, 447 pg L-1, and 0.67 pg m-3 in SW, the SML and SSA, respectively. The enrichment factors of PFAS in the SML and SSA ranged between 1.2 and 5, and between 522 and 4690, respectively. This amplification of concentrations in the SML is consistent with the surfactant properties of PFAS, while the large enrichment of PFAS in atmospheric SSA may be facilitated by the large surface area of SSA and the sorption of PFAS to aerosol organic matter. This is the first field work assessing the simultaneous occurrence of PFAS in SW, the SML and SSA. The large measured amplification of concentrations in marine aerosols supports the role of SSA as a relevant vector for long-range atmospheric transport of PFAS.

Involvement of mitochondrial permeability transition, glutathione status, pentose phosphate pathway and oxidative damage in the protective effect of fasting on the ischaemic-reperfused rat heart.

1. Fasting, which increases the catabolism of fatty acids, gives functional protection to the ischaemic-reperfused heart. To obtain further knowledge of this cardioprotective effect, changes in mitochondrial permeability transition (MPT) were measured by the entrapment of 2-deoxy-[(3)H]-glucose (2-DG). We also assessed whether MPT is associated with changes in glutathione status, the activity of glucose-6-phosphate-dehydrogenase (G6PDH) and tissue oxidative damage, estimated by the measurement of Thiobarbituric acid-reactive substances (TBARS). 2. Spontaneously beating hearts of fed and 24 h fasted rats were Langendorff perfused with Krebs'-Ringer bicarbonate solution (10 mmol/L glucose) and exposed to 25 min global ischaemia, followed by 30 min reperfusion. 3. Ischaemia-reperfusion resulted in a fourfold increase in mitochondrial entrapment of 2-DG in the fed group. This response was 29% lower in the fasted group, but there were no concomitant changes in total retention of 2-DG in the heart. Fasting increased the activity of G6PDH by a factor of 1.4 and caused a 2.8-fold increase in the ratio of reduced glutathione to oxidized glutathione (GSH:GSSG) at the end of the pre-ischaemic period. Ischaemia-reperfusion did not affect G6PDH activity, but reduced the GSH:GSSG ratio in both the fed and fasted groups by 50%. Therefore, the GSH:GSSG ratio remained higher in the fasted group. Fasting also decreased cellular levels of TBARS by approximately 25%. Lipolysis of endogenous triacylglycerol was increased during the pre-ischaemic period in the fasted group. 4. These data suggest that the enhancement of fatty acid catabolism that occurs in fasting activates mechanisms that tend to reduce oxidative damage and limit MPT.

Protection of ischaemic-reperfused rat heart by dimethylamiloride is associated with inhibition of mitochondrial permeability transition.

1. The aim of the present study was to assess whether protection afforded by the Na(+)/H(+) exchanger blocker dimethylamiloride (DMA) is associated with inhibition of mitochondrial permeability transition (MPT). The effects of DMA were compared with those of cyclosporine (Cs) A, an inhibitor of MPT. 2. Rat hearts were Langendorff perfused with Krebs'-bicarbonate medium containing 10 mmol/L glucose and were subjected to 25 min no-flow global ischaemia and 30 min reperfusion in the presence or absence of 10 micromol/L DMA or 0.2 micromol/L CsA. Cell viability was measured using tetrazolium stain. The MPT was determined by loading hearts with 2-deoxy-[(3)H]-glucose (2DG), which enters mitochondria only during MPT. Total heart 2DG content as an estimation of the extent of tissue damage was also measured. To assess whether DMA has any direct effect on glycolysis, a cell-free heart extract containing all the glycolytic enzymes was used. 3. Dimethylamiloride improved functional recovery (rate-pressure product) from 24 +/- 7 to 68 +/- 11% (P < 0.01) at reperfusion end, attenuated the increase in left ventricular end-diastolic pressure (from 29 +/- 7 to 6 +/- 3% 10 min after reperfusion onset; P < 0.01), improved cell viability (from 21.2 +/- 6.6 to 69.6 +/- 7.1% at reperfusion end; P < 0.05) and lessened lactate accumulation at the end of ischaemia (119 +/- 15 vs 163 +/- 14 micromol/g dry weight; P < 0.05). Dimethylamiloride limited MPT: 2DG mitochondrial entrapment, being 33.1 +/- 14.2 and 96.3 +/- 14.0 at reperfusion end in the treated and control hearts, respectively (P < 0.05), and concomitantly raised total 2DG content (51.3 +/- 4.4 vs 86.8 +/- 1.7 x 10(3) d.p.m./g wet weight in control and treated groups, respectively; P < 0.05). Cyclosporine A improved functional recovery and attenuated the amplitude of ventricular diastolic pressure in ischaemic-reperfused hearts. It also reduced mitochondrial entrapment (67.3 +/- 7.7%; P < 0.05 vs control) and increased total cell 2DG content (162.3 +/- 1.3 x 10(3) d.p.m./g wet weight; P < 0.01 vs control) at the end of reperfusion. Dimethylamiloride did not affect glucose consumption and lactate production in the cell-free heart extract. 4. In conclusion, DMA protects against the noxious effects of ischaemia-reperfusion and inhibits MPT, coinciding with present and previous findings concerning the effects of CsA. Dimethylamiloride also diminished lactate accumulation, although it did not exhibit any direct effect on glycolysis. These data suggest that blockade of Na(+)/H(+) exchange by DMA attenuates the extent of MPT in ischaemic-reperfused rat heart.

Role of endogenous nitric oxide in classic preconditioning in rat hearts.

Ischemic preconditioning (IPC) protects the heart against subsequent sustained ischemia reperfusion (RP). Despite many triggers and signaling pathways, which seem to be involved in IPC, the IPC-mechanisms remain a controversial issue. One of them is endogenous production of nitric oxide (NO). To assess the role of NO in IPC and its relation with glycogen and glycolysis, the effects of inhibiting NO synthase with L-NAME (50 microM) were examined in IPC rat hearts perfused with medium containing 10 mM glucose. Left ventricular developed pressure-rate product (RPP) and end diastolic pressure (EDP), lactate and glycogen contents, and cell viability were measured. Global ischemia (25 min) was followed by 30 min RP. IPC consisted in one cycle of 3 min ischemia-5 min RP. IPC reduced EDP and improved RP recovery of RPP. L-NAME had no effects on the non-IPC group but abolished these effects of IPC. IPC reduced ischemic decrease of glycogen and the acceleration of glycolysis, and improved cell viability. L-NAME did not affect these effects of IPC. The results suggest that NO is ineffective on the noxious effects of ischemia-RP in non-IPC hearts and on the effects of IPC on cell viability, glycogenolysis and glycolysis whereas it is only involved in functional protection.

Effects of wortmannin on cardioprotection exerted by ischemic preconditioning in rat hearts subjected to ischemia-reperfusion.

Ischemic preconditioning (IPC) is one of the most powerful interventions to reduce ischemia-reperfusion injury. The aim of the present study was to investigate the involvement of the phosphatidylinositol-3-kinases (PI3Ks) family in cardioprotection exerted by IPC and the relationship between preservation of mitochondrial morphology and ATP synthesis capacity. In this regard, macroautophagy (autophagy) is considered a dynamic process involved in the replacement of aged or defective organelles under physiological conditions. IPC consisted of four 5-min cycles of ischemia-reperfusion followed by sustained ischemia. Wortmannin (W), a PI3K family inhibitor, was added to the perfusion medium to study the involvement of autophagy in the beneficial effects of IPC. In the present study, LC3-II/I expression was significantly increased in the IPC group when compared with the control group. The hearts subjected to IPC showed greater degradation of p62 than control groups, establishing the existence of an autophagic flow. Electron microscopy showed that IPC preserves the structural integrity of mitochondria after ischemia and at the end of reperfusion. Moreover, hearts subjected to IPC exhibited increased mitochondrial ATP synthesis. The beneficial effects of IPC were abolished by W in all trials of this study, abolishing the differences between the IPC and control groups. These results suggest that IPC could partly reduce injury by ischemia-reperfusion (I/R) by decreasing mitochondrial damage and promoting autophagy. Since W is a nonspecific inhibitor of the PI3Ks family, further research is required to confirm participation of PI3K in the response to IPC.

Estado dental y periodontal de población en tratamiento por consumo de drogas: Estudio piloto / Dental and periodontal condition of a population in treatment for drug use: Pilot study

El uso problemático de drogas puede afectar la salud oral de los consumidores. El presente estudio pretendió detectar la prevalencia de patología dentaria y periodontal en una población adolescente y adulta joven en tratamiento por drogo-dependencia. Se diseñó un estudio transversal, observacional y descriptivo, incluyendo a 72 individuos que se asisten por su adicción en el Portal Amarillo, centro de referencia nacional. La media del índice CPOD fue de 8,04. Al discriminar por franja etaria, la comprendida entre 15 y 24 años tuvo un CPOD de 5,31, mientras que la comprendida entre 25 y 35 años tuvo un valor de 11,27. El relevamiento paradencial mostró que el 65% de los participantes presentaron gingivitis y el 18% cuadros de periodontitis. Los resultados obtenidos mostraron que existe una mayor prevalencia de enfermedad oral en pacientes drogo-dependientes que la población general. Los servicios de salud del primer nivel deberían desarrollar acciones especiales de prevención y detección precoz en pacientes drogo-dependientes...

Problematic drug use may affect the oral health of consumers. This research was designed to detect the prevalence of dental and periodontal pathology in an adolescent and young adult population in treatment for drug dependence. A transversal, observational, descriptive study was conducted. It included 72 subjects being treated for drug addiction at Portal Amarillo, a national reference centre. The mean value of the DMF index was 8.04. When discriminating by age group, in the ages between 15 and 24 the DMF Index was 5.31, while in the ages between 25 and 35 it was 11.27. The periodontal survey showed that 65% of the participants suffered from gingivitis and 18% from periodontitis. The results showed a greater prevalence of oral disease in patients who are drug addicts than in the rest of the population. First level health services should take special prevention and early detection measures when treating patients who are drug addicts...

Effects of wortmannin on cardioprotection exerted by ischemic preconditioning in rat hearts subjected to ischemia-reperfusion

Ischemic preconditioning (IPC) is one of the most powerful interventions to reduce ischemia-reperfusion injury. The aim of the present study was to investigate the involvement of the phosphatidylinositol-3-kinases (PI3Ks) family in cardioprotection exerted by IPC and the relationship between preservation of mitochondrial morphology and ATP synthesis capacity. In this regard, macroautophagy (autophagy) is considered a dynamic process involved in the replacement of aged or defective organelles under physiological conditions. IPC consisted of four 5-min cycles of ischemia-reperfusion followed by sustained ischemia. Wortmannin (W), a PI3K family inhibitor, was added to the perfusion medium to study the involvement of autophagy in the beneficial effects of IPC. In the present study, LC3-II/I expression was significantly increased in the IPC group when compared with the control group. The hearts subjected to IPC showed greater degradation of p62 than control groups, establishing the existence of an autophagic flow. Electron microscopy showed that IPC preserves the structural integrity of mitochondria after ischemia and at the end of reperfusion. Moreover, hearts subjected to IPC exhibited increased mitochondrial ATP synthesis. The beneficial effects of IPC were abolished by W in all trials of this study, abolishing the differences between the IPC and control groups. These results suggest that IPC could partly reduce injury by ischemia-reperfusion (I/R) by decreasing mitochondrial damage and promoting autophagy. Since W is a nonspecific inhibitor of the PI3Ks family, further research is required to confirm participation of PI3K in the response to IPC (AU)

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