EFECTO DE LA DEFICIENCIA DE ZINC EN LA EXPRESIÓN DE PARÁMETROS DE INJURIA PULMONAR

BIAGGIO, V; ALVAREZ, SM; GATICA, LV; GOMEZ, N; GIMENEZ, MS.

Misiones

Congreso; SOCIEDAD ARGENTINA DE INVESTIGACION CIENTÍFICA y BIOLÓGICA (SAIB); 2004

SOCIEDAD ARGENTINA DE INVESTIGACION CIENTÍFICA y BIOLÓGICA (SAIB)

ABSTRACT Zinc is a micronutrient whose deficiency is associated with oxidative stress. Besides, nitric oxide (NO) plays an important role in the pulmonary physiology, but the expression of the inducible isoform of the enzyme that synthesizes NO (iNOS) is presented in lung injury. It is known that PPARã and TGF-â1 are factors whose expression is related to inflammatory situations. To evaluate the effect of lung injury in the chronic Zinc deficiency we studied the expression of iNOS, PPARã and TGF-â1 in rat lung. Wistar male rats (200 ± 20 g) were fed with AIN-93 diet (zinc deficient, ZD) or with 30 mg Zn/ kg (Control, Co) during 2 months. Total RNA was isolated from lung by using TRIzol. 1 µg of RNA was transcribed to cDNA at 42°C using random hexamers as primers and RT-MMLV (Moloney Murine Leukemia Virus). Aliquots of 2 µl of cDNA were used in the amplifications by PCR using specific primers for the following genes: iNOS and PPARã. Beta actin was used as an internal control. 100 mg of lung were homogenized in the presence of protease inhibitors and 40 µg of proteins were separated in an 10% SDS-PAGE, transferred to PVDF membranes and incubated with an antibody against TGF- â1. The bands were quantified by densitometry. We detected a significant increase in iNOS (p< 0.001) and TGF- â1 (p<0.01) while PPARã decreased significantly (p< 0.05). These results confirm an inflammatory situation under chronic Zinc deficiency.