A comparison between expresion of Heme oxygenase and Nitric Oxyde Synthase in brain of mice treated with porphyrinogenic agents. Immunohistochemical studies.

BUZALEH, ANA MARIA; MEISS, ROBERTO; VALLECORSA, PABLO; LAVANDERA, JIMENA; RUSPINI, SILVINA; BATLLE, ALCIRA

Edimburgo

Congreso; 7th INTERNATIONAL CONGRESS ON HEME OXYGENASES AND RELATED ENZYMES; 2012

Hemeoxygenase-1 (HO-1) degrades heme; it is sensitive to stimuli and agents that cause oxidative stress and pathological conditions, ranging from Alzheimer to cancer. HO-1 expression is often boosted in tumour tissues and further elevated in response to photodynamictherapy. Nitric Oxide Synthase (NOS), a family of four isoforms: endothelial (eNOS), neuronal (nNOS), inducible (iNOS), mitochondrial (mtNOS), synthesize nitric oxide (NO) which has neuronal, glial and vascular physiological effects and it is involved in neurodegenerative diseases. We observed thatporphyrinogenic agents affect the brain mice activity and expression of HO and NOS depending on the drug assayed. The aim was to compare the effects of anaesthetics: Enflurane, Isoflurane, and other porphyrinogenic agents: allisisopropilacetamide (AIA), veronal, ethanol, on the expression of HO-1 and NOS isoforms in different mice brain cells. Fixed brains(10% neutralbuffered formalin) were embedded in paraffin. Immunohistochemistry was performed using streptavidinbiotin-peroxidase complex system LSAB (DAKO).Control mice showed expression of n-NOS, i-NOS and HO-1 in neurons; e-NOS was only detected in vessels. In neurons, nNOS expression was augmented by all the xenobiotics assayed; iNOS was only increased after anaesthetics, Veronal and ethanol and eNOS after anaesthetics and AIA treatments. HO-1 expression was also induced in neurons of all studied groups. Interestingly, iNOS and HO-1 expression in brain choroid plexus and glial cells was positive in the majority of treated groups. A good correlation between HO-1 and iNOS response was observed in neurons. All NOS isoforms were induced by porphyrinogenic agents being more significant in glial cells for iNOS.