Zinc aspartate alleviates lung injury induced by intestinal ischemia-reperfusion in rats

Intestinal ischemia-reperfusion (II/R) induced acute lung injury is mediated by activated neutrophils and formation of free radicals. Several antioxidants have been shown to attenuate such remote organ injury. We studied the effects of zinc aspartate on lung injury induced by II/R in rats.

Twenty-four Sprague-Dawley rats were randomized into three groups. Group I was the control. Animals in Groups II and III (II/R + zinc aspartate [ZA]) underwent 60 min of ischemia and 60 min of reperfusion, respectively. Rats in Group III also received 50 mg/kg zinc aspartate before 15 min of reperfusion. Lung tissue samples and bronchoalveolar lavage fluid were obtained to assess lung tissue myeloperoxidase (MPO), adenosine deaminase (ADA), xanthine oxidase (XO), glutathione peroxidase (GPx) activities, and nitric oxide (NO), malondialdehyde (MDA) levels. Also, the levels of MDA, NO, and MPO activity were determined in bronchoalveolar lavage fluid.

Compared with the control, lung tissue MDA, NO levels, and MPO, ADA, XO activities were markedly increased (P < 0.05), whereas GPx activity significantly decreased in the II/R group (P < 0.05). However, administration of ZA significantly reversed these effects by reducing the levels of MDA, NO, and decreasing MPO, ADA, XO activities (P < 0.05). In addition, ZA significantly increased GPx activity (P < 0.05). The activity of MPO and the levels of NO and MDA were found to be higher in bronchoalveolar lavage fluid in II/R group than the control (P < 0.05). Zinc aspartate significantly diminished MPO activity and the levels of NO and MDA compared with that of control rats (P < 0.05).

Our results indicate that zinc aspartate alleviates lung injury induced by II/R attributable to its antioxidant and antiinflammatory effects.