Mario Marino

Lipid Peroxidation, Tissue Necrosis, and Metabolic and Mechanical Recovery of Isolated Reperfused Rat Heart as a Function of Increasing Ischemia

Isolated Langendorff-perfused rat hearts, after 30 min of preperfusion, were submitted to increasing times of global normothermic ischemia (1, 2, 5, 10, 20 and 30 min) or to the same times of ischemia followed by 30 min of reperfusion. Analysis of malondialdehyde, ascorbic acid, oxypurines, nucleosides, nicotinic coenzymes and high-energy phosphates was carried out by HPLC on neutralized perchloric acid extracts of freeze-clamped tissues. In addition, maximum rate of intraventricular pressure development and cardiac output of malondialdehyde, lactate dehydrogenase, oxypurines and nucleosides were monitored during both preperfusion and reperfusion. Besides decreasing energy metabolites and nicotinic coenzyme pool, prolonged ischemia produced oxidation of significant amounts of hypoxanthine and xanthine to uric acid and generation of detectable levels of malondialdehyde (0.002 micromol/g dry weight). After oxygen and substrate readmission, tissue and perfusate malondialdehyde increased only if previous ischemia was longer than 5 min, while lactate dehydrogenase was detected in perfusate of reperfused hearts following 10, 20, and 30 min of ischemia. Highest values of tissue malondialdehyde and total malondialdehyde output were recorded in reperfused hearts subjected to 30 min of ischemia (0.043 micromol/g dry weight and 0.069 micromol/30 min/g dry weight, respectively). Since tissue malondialdehyde was observed without detectable lactate dehydrogenase release in perfusate, it might be stated that malondialdehyde generation (i.e., lipid peroxidation) temporally preceded lactate dehydrogenase release (i.e., tissue necrosis). In reperfused hearts, evaluation of myocardial energy state and of mechanical recovery allowed us to determine times of ischemia beyond which reperfusion did not positively affect these metabolic and functional parameters. Main findings are that, under these experimental conditions, lipid peroxidation might be the cause and not the consequence of tissue necrosis and that duration of ischemia might be the factor deciding effectiveness of reperfusion.

Cloning and chromosomal localization of a cDNA encoding a mitochondrial porin from Drosophila melanogaster

We have raised polyclonal antibodies against purified the Drosphila melanogaster mitochondrial porin. They showed high titre and specificity and were thus used as a tool for screening an expression library. The isolated clone 1T1 showed 74% sequence identity in the last 19 residues at the C‐terminus of human porin. A subclone of 1T1, containing the porin‐like sequence, was thus used as a probe for re‐screening a cDNA library and several positive clones were plaque‐purified. We present here the sequence of a 1363 bp cDNA encoding a protein of 279 amino acids. Its identity with porin was also confirmed by N‐terminal Edman degradation of the purified protein. The D. melanogaster porin shows an overall 51.8% identity with human porin isoform 1 (porin 31HL or HVDAC1) and an overall 55.7% identity with human porin isoform 2 (HVDAC2). Hydrophobicity plots and secondary structure predictions showed a very high similarity with data obtained from known porin sequences. The D. melanogaster porin cDNA was used as a probe for in situ hybridization to polytenic salivar gland chromosomes. It hybridizes with different intensities in two sites, in chromosome 2L, at region 31E and in chromosome 3L at region 79D. Thus, also in Drosophila melanogaster porin polypeptide(s) belong(s) to a multigene family.

Lp theory and partial Hölder continuity for quasilinear parabolic systems of higher order with strictly controlled growth

SuntoSia μ ε L2(−T, 0, Hm(Ω, RN)) ∩ L∞(−T, 0, L2(Ω, RN)) una soluzione in Q=Ω x x (−T, 0) del sistema quasi-lineare parabolico di ordine 2m

275-01275-01275-01Regularity of the spatial derivatives of the solutions to parabolic systems in divergence form

\begin{gathered} ( - 1)^m \mathop \sum \limits_{\left| \alpha \right| = m} \mathop \sum \limits_{\left| \beta \right| = m} D^\alpha (A_{\alpha \beta } (X, \delta u)D^\beta u) + \frac{{\partial u}}{{\partial t}} = \hfill \\ = ( - 1)^m \mathop \sum \limits_{\left| \alpha \right| = m} D^\alpha f^\alpha (X, \delta u) + \mathop \sum \limits_{\left| \alpha \right| \leqslant m - 1} ( - 1)^{\left| \alpha \right|} D^\alpha f^\alpha (X, Du). \hfill \\ \end{gathered}

Modelling the three-dimensional structure and the electrostatic potential field of two Cu,Zn superoxide dismutase variants from tomato leaves

In questa Nota, nella ipotesi che i vettorifα abbiano i seguenti andamenti controllati

Differentiability of weak solutions of nonlinear parabolic systems with quadratic growth

\begin{gathered} \left\| {f^\alpha (X,\delta u)} \right\| \leqslant g^\alpha (X) + c\mathop \sum \limits_{\left| \beta \right| \leqslant m - 1} \left\| {D^\beta u} \right\|^{\theta (m,\left| \beta \right|)} ,\left| \alpha \right| = m, \hfill \\ \left\| {f^\alpha (X,Du)} \right\| \leqslant g^\alpha (X) + c\mathop \sum \limits_{\left| \beta \right| \leqslant m} \left\| {D^\beta u} \right\|^{\theta (\left| \alpha \right|,\left| \beta \right|)} ,\left| \alpha \right| \leqslant m - 1, \hfill \\ \end{gathered}