PAHs in franciscana dolphins from the Southwestern Atlantic Ocean: Concentration and maternal transfer assessments.

Polycyclic aromatic hydrocarbons (PAHs) are organic compounds ubiquitous in the environment and known for their toxic, mutagenic, and carcinogenic effects. These compounds can bioaccumulate in the biota and be transferred through trophic webs. The franciscana dolphin (Pontoporia blainvillei), as top predators, can be an environmental sentinels. Thus, this study aimed to provide data about PAHs concentration in their hepatic tissue collected on the coast of Espírito Santo (Franciscana Management Area, FMA Ia), Rio de Janeiro (FMA IIa), and São Paulo states (FMA IIb), in Southeastern Brazil. PAHs were detected in 86 % of franciscana dolphins (n = 50). The highest ∑PAHsTotal median concentration was reported in FMA Ia followed by FMA IIb and FMA IIa (1055.6; 523.9, and 72.1 ng.g-1 lipid weight, respectively). Phenanthrene was detected in one fetus and two neonates, showing maternal transfer of PAHs in these dolphins. Evaluating PAHs with potential toxic effects is of utmost importance for the conservation of a threatened species.

A baseline evaluation of PAH body burden in sardines from the southern Brazilian shelf.

The concentrations of 37 polycyclic aromatic hydrocarbons (PAHs) and their potential risk to human health were determined in fifty sardine muscle (Sardinella brasiliensis) samples collected along the southern Brazilian shelf. Parental and alkylated PAHs were identified and quantified using a pressurized liquid extraction with in-cell purification method and gas chromatography-mass spectrometry identification and quantification. The concentrations of Σ37 PAHs in muscle ranged between 6.02 and 4074 µg kg-1 wet weight, which are comparable to levels reported for commercially important fish worldwide. The most abundant compounds were pyrene and fluoranthene, which originate from both petrogenic and pyrolytic hydrocarbon inputs. In only 4% of the samples the benzo[a] pyrene equivalent concentration was above the threshold of 6 µg kg-1 suggested for safe fish consumption in Brazil. These findings will serve as baseline data for monitoring the quality of sardines consumed in the country and for studying fish populations.

Mitochondrial K+ transport and cardiac protection during ischemia/reperfusion.

Mitochondrial ion transport, oxidative phosphorylation, redox balance, and physical integrity are key factors in tissue survival following potentially damaging conditions such as ischemia/reperfusion. Recent research has demonstrated that pharmacologically activated inner mitochondrial membrane ATP-sensitive K+ channels (mitoK(ATP)) are strongly cardioprotective under these conditions. Furthermore, mitoK(ATP) are physiologically activated during ischemic preconditioning, a procedure which protects against ischemic damage. In this review, we discuss mechanisms by which mitoK(ATP) may be activated during preconditioning and the mitochondrial and cellular consequences of this activation, focusing on end-effects which may promote ischemic protection. These effects include decreased loss of tissue ATP through reverse activity of ATP synthase due to increased mitochondrial matrix volumes and lower transport of adenine nucleotides into the matrix. MitoK(ATP) also decreases the release of mitochondrial reactive oxygen species by promoting mild uncoupling in concert with K+/H+ exchange. Finally, mitoK(ATP) activity may inhibit mitochondrial Ca2+ uptake during ischemia, which, together with decreased reactive oxygen release, can prevent mitochondrial permeability transition, loss of organelle function, and loss of physical integrity. We discuss how mitochondrial redox status, K+ transport, Ca2+ transport, and permeability transitions are interrelated during ischemia/reperfusion and are determinant factors regarding the extent of tissue damage.

Carvedilol: just another Beta-blocker or a powerful cardioprotector?

Beta-blockers have been used to treat ischemic heart disease, due to negative chronotropic and inotropic properties, thus inducing a decrease in myocardial consumption of oxygen and nutrients, allowing a better balance between nutritional needs and the supply provided by the coronary blood flow. Recent developments in cell biology allowed us to understand that not all beta-blockers are equal, as their intracellular mechanisms of action can be very different. This paper will focus on carvedilol, a non-selective beta-blocker with alfa-blocker properties, currently used to treat hypertension, heart failure and coronary artery disease. Effects of carvedilol on cardiac mitochondria, their relation to its antioxidant properties, and how these can improve cardiomyocyte resistance to aggression and cardiac function will be discussed. We will begin by depicting the effect of carvedilol on mitochondrial parameters, namely oxidative phosphorylation, calcium homeostasis and energy production. Then we will focus on the mitochondrial permeability transition (MPT) and how the antioxidant properties of carvedilol can be used to minimize oxidative stress, a powerful inducer of MPT. Carvedilol will also be highlighted as an enzyme modulator, focusing on its importance to prevent doxorubicin (DOX) cardiotoxicity. The mitochondrial-related mechanism of cardioprotection involving carvedilol will also be addressed, as we will discuss some clinical pieces of evidence showing the importance of mechanisms previously depicted. In conclusion, based upon its molecular mechanisms of action, carvedilol seems to be a unique beta-blocker. These unique characteristics can help us understand the positive impact of carvedilol on the prognosis of patients with heart disease.

Mitochondrial K+ transport and cardiac protection during ischemia/reperfusion

Mitochondrial ion transport, oxidative phosphorylation, redox balance, and physical integrity are key factors in tissue survival following potentially damaging conditions such as ischemia/reperfusion. Recent research has demonstrated that pharmacologically activated inner mitochondrial membrane ATP-sensitive K+ channels (mitoK ATP) are strongly cardioprotective under these conditions. Furthermore, mitoK ATP are physiologically activated during ischemic preconditioning, a procedure which protects against ischemic damage. In this review, we discuss mechanisms by which mitoK ATP may be activated during preconditioning and the mitochondrial and cellular consequences of this activation, focusing on end-effects which may promote ischemic protection. These effects include decreased loss of tissue ATP through reverse activity of ATP synthase due to increased mitochondrial matrix volumes and lower transport of adenine nucleotides into the matrix. MitoK ATP also decreases the release of mitochondrial reactive oxygen species by promoting mild uncoupling in concert with K+/H+ exchange. Finally, mitoK ATP activity may inhibit mitochondrial Ca2+ uptake during ischemia, which, together with decreased reactive oxygen release, can prevent mitochondrial permeability transition, loss of organelle function, and loss of physical integrity. We discuss how mitochondrial redox status, K+ transport, Ca2+ transport, and permeability transitions are interrelated during ischemia/reperfusion and are determinant factors regarding the extent of tissue damage.