HYPEROXIA INDUCES INTERSTITIAL (TYPE-I) AND INCREASES TYPE-IV COLLAGENASE MESSENGER-RNA EXPRESSION AND INCREASES TYPE-I AND TYPE-IV COLLAGENOLYTIC ACTIVITY IN NEWBORN RAT LUNG

Oxygen toxicity is attributed to the reaction of oxygen metabolites wi th cellular components leading to cell destruction. Activation of late nt human neutrophil interstitial collagenase by reactive oxygen specie s has been demonstrated. The potential role of collagenases in hyperox ic lung injury has not been investigated. We studied the effect of hyp eroxia on newborn rat lung water content, morphology and ultrastructur e, interstitial (type I) and type IV collagenase gene expression and t ype I and IV collagenolytic activity. We observed that hyperoxia cause s pulmonary edema, alters newborn rat lung morphology in a sequential manner and produces ultrastructural alterations, induces type I and in creases type IV collagenase mRNA expression, and increases type I and IV collagenolytic activity. A role for type I and IV collagenase in hy peroxic newborn lung injury or in the recovery following the injury is proposed.