2007 Volume 24 Pages 133-138
Zinc (Zn) is an essential trace element and a cofactor of over 300 enzymes. Various symptoms such as growth retardation and dermatitis are associated with Zn deficiency. In recent years, it has been suggested that Zn deficiency causes alteration in the biological defense system. To investigate effects of Zn deficiency on lungs, we examined morphological changes and expression of TNF-α mRNA in the lung tissue after high pressure exposure to oxygen. In the present study, two special diets were prepared; a Zn deficient diet and a standard diet (0.01 % Zn). Seven- weeks-old SD strain male rats were fed either on a Zn deficient (Zn-D group, n = 16) or a standard (Control group, n = 16) diets for 5 weeks. Eight of 16 Zn-D rats and 8 of 16 Control rats were exposed to 2 ATA pure oxygen for 5 hours (ZnD-O2 and Control-O2 groups). Then, determination of the number of white blood cells (WBC) and serum CRP level, histopathological examination of lung tissue and detection of TNF-α expression in the tissue were carried out.
Severe pathological changes such as congestion, destruction of alveoli and the appearance of inflammatory cells were seen in ZnD-O2 rats, suggesting that Zn deficiency reduces the threshold level of oxygen toxicity in the pulmonary tissue. On the other hand, increase in TNF-α mRNA was not detected in ZnD-O2 animals, although severe damage in the lung was observed. Further studies including localization of TNF-α mRNA expression within the tissue are required to clarify the mechanism of the synergistic effects of Zn deficiency on the lung lesions caused by inhalation of high pressure oxygen.
