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Reactive oxygen species (ROS) play an important role in neuronal damage and death that occurs in several neurodegenerative disorders, namely in Alzheimer's disease (AD). The observation that ROS neutralization may slow or reduce the neurodegenerative process associated with those pathologies stimulates the development of new drugs, more efficient and well tolerated, with antioxidant properties. Vinpocetine [14-etoxicarbonyl-3alpha,16alpha-ethyl)-14,15-eburnamine], a vincamine derivative, efficiently protects cells from ROS attack. Recently, the protective effect of vinpocetine was demonstrated using in vitro models of oxidative stress induced by the oxidant pair ascorbate/Fe2+ and by synthetic peptides of the AD-associated b-amyloid protein (Abeta). Results obtained from these in vitro experiences support that additional clinical trials should be carried out using vinpocetine, or vinpocetine derivatives, in order to test its therapeutical or preventive effects in diseases where oxidative stress plays a crucial role.

Objectives: A growing number of reports in the literature have been correlating cardiovascular alterations with the presence of chronic liver disease, such as cirrhosis and cholestasis. The objective of this work was to compare mitochondrial bioenergetics and calcium loading capacity in the hearts of rats injected with alpha-naphthylisothiocyanate (ANIT), a compound used to induce cholestasis in animal models., Methods: Female Wistar rats (n = 12) were randomly divided into two groups. One of the groups was injected with six weekly doses of ANIT. Each group was evaluated in terms of mitochondrial bioenergetic capacity and susceptibility to the mitochondrial permeability transition (MPT), a deleterious phenomenon associated with oxidative stress and excessive mitochondrial calcium accumulation., Results: Our data showed unequivocally that cardiac mitochondria of rats chronically injected with ANIT lost their ability to accumulate calcium, in a cyclosporin A sensitive manner. This was reflected in a higher calcium-dependent swelling rate and amplitude (p < 0.01). The RCI value, an index of mitochondrial integrity, was also lower in the ANIT-treated group (p < 0.05)., Conclusions: This suggests that during cholestasis development, cardiac mitochondria lose their normal ability to control cytosolic calcium due to increased susceptibility to the MPT. Our results may suggest an explanation for the occurrence of cardiomyopathies associated with cholestatic disease, which may persist even in the absence of serum markers for liver disease.

Diabetes is one of the most common metabolic diseases of our times. Specific cardiovascular alterations are often associated with the progression of this disease. Considerable controversy exists in the literature concerning the greater or lesser susceptibility of the diabetic heart to ischemia and reperfusion. Cardiac mitochondria may be fundamental to the differential susceptibility of the cardiomyocyte to pathologic phenomena, particularly those due to the induction of the degenerative process known as the mitochondrial permeability transition (MPT), which is triggered by excessive mitochondrial calcium accumulation. The MPT has been associated with cellular dysfunction resulting from ischemia and reperfusion. The objective of this work was to examine the susceptibility of mitochondria isolated from diabetic rats to the MPT, in comparison to healthy control rats of the same age. Cardiac mitochondria from the diabetic rats had higher calcium loading capacity before the development of the MPT, with a decreased incidence of MPTP-associated features. This was associated with a greater capacity to sustain multiple pulses of externally added calcium, simultaneously with maintenance of the transmembrane electrical potential and reduced swelling amplitude. This could mean that cardiomyocytes from diabetic hearts may indeed be less prone to dysfunctions resulting from ischemia and reperfusion, at least in milder diabetic conditions, thus explaining many reports in the literature.