M. Rodríguez, B. Buchholz, V. D’Annuzio, M. Donato, G.E. González, M. A. Goyeneche, T. Mazo, V. Pérez, L. Wilensky, R.J. Gelpi^*

BIOCELL, Vol.40, No.1, pp. 43-46, 2016, DOI:10.32604/biocell.2016.40.043

Abstract Dystrophin is a membrane-associated protein responsible for structural stability of the sarcolemma in cardiac myocytes and is very sensitive to ischemic damage. The goal of our study was to determine if ischemic preconditioning could prevent dystrophin breakdown through inhibition of matrix metalloproteinase-2 (MMP-2) activity. Isolated rabbit hearts were subjected to global ischemia with or without reperfusion in order to evaluate if dystrophin is preserved by ischemic preconditioning through MMP-2 inhibition. Ischemic preconditioning significantly reduced the infarct size induced by 30 min of ischemia and 180 min of reperfusion. Importantly, it also diminished dystrophin proteolysis and More >

S.S. Bombicino^*, D.E. Iglesias, I.A. Rukavina Mikusic, A. Boveris, L.B. Valdez

BIOCELL, Vol.40, No.1, pp. 7-10, 2016, DOI:10.32604/biocell.2016.40.007

Abstract Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. Alterations in the contractile response and lusitropic reserve were observed in streptozotocin diabetic rats after β-adrenergic stimuli. Additionally,… More >

BIOCELL, Vol.40, Suppl.S, pp. 9-10, 2016

Abstract This article has no abstract. More >

BIOCELL, Vol.40, Suppl.S, pp. 7-8, 2016

Abstract This article has no abstract. More >

BIOCELL, Vol.40, Suppl.S, pp. 5-6, 2016

Abstract This article has no abstract. More >

BIOCELL, Vol.40, Suppl.S, pp. 3-4, 2016

Abstract This article has no abstract. More >

BIOCELL, Vol.40, Suppl.S, pp. 1-2, 2016

Abstract This article has no abstract. More >

Tamara ZAOBORNYJ, Darío E. IGLESIAS, Silvina S. BOMBICINO, Alberto BOVERIS, Laura B. VALDEZ^*

BIOCELL, Vol.40, No.1, pp. 55-58, 2016, DOI:10.32604/biocell.2016.40.055

Abstract Normal cardiac function is accomplished through a continuous energy supply provided by mitochondria. Heart mitochondria are the major source of reactive oxygen and nitrogen species: superoxide anion (O₂-) and nitric oxide (NO). NO production by mitochondrial NOS (mtNOS) is modified by metabolic state and shows an exponential dependence on Δψ. The interaction between mtNOS and complexes I and IV might be a mechanism involved in the regulation of mitochondrial NO production. NO exerts a high affinity, reversible and physiological inhibition of cytochrome c oxidase activity. A second effect of NO on the respiratory chain is accomplished More >

Claudia G. REIDES^1,2, Romina M. LASAGNI VITAR^1,2, Agustina PEVERINI¹, Natasha S. JANEZIC¹, Ailen G. HVOZDA ARANA¹, Sandra M. FERREIRA^1,2, Susana F. LLESUY^1,2*

BIOCELL, Vol.40, No.1, pp. 51-54, 2016, DOI:10.32604/biocell.2016.40.051

Abstract The purpose of this study was to evaluate the redox status changes of primary visual targets in the rat brain of a high pressure-induced glaucoma model. The animal model consisted of inducing ocular hypertension by cauterizing two episcleral veins on the left eye. The markers of oxidative damage and the oxidative balance evaluated in the brain seven days postoperative were: nitrites concentration, levels of non-enzymatic antioxidants and antioxidant enzymes activity.
The increase in the nitrite content, which could be the result of the enhancement in the production of nitrogen species, and in the activity of NADPH… More >

Virginia VANASCO, Timoteo MARCHINI, Natalia MAGNANI, Tamara VICO, Mariana GARCES, Lourdes CACERES, Alejandro GUAGLIANONE, Pablo EVELSON, Silvia ALVAREZ.^*

BIOCELL, Vol.40, No.1, pp. 47-50, 2016, DOI:10.32604/biocell.2016.40.047

Abstract Several authors have addressed the importance of mitochondrial function in inflammatory syndromes, as it may play a role in the genesis of tissue injury. Sepsis and exposition to environmental particles are examples of inflammatory conditions. Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes. One of the current hypotheses for the molecular mechanisms underlying the complex condition of sepsis is that enhanced NO production and oxidative stress lead to mitochondrial dysfunction, bioenergetic derangement and organ failure. The mechanism of particulate matter-health effects are believed to involve inflammation and oxidative More >