Background : Pulmonary damage resulting from lipid peroxidation is a principal effect of paraquat intoxication. The host-defense functions of surfactant are known to be mediated by the surfactant proteins A and D (SP-A and SP-D, respectively). The primary objective of this study was to evaluate the variations over time in levels of surfactant protein and lipid peroxidation (LPO) in lung tissue following free-radical-induced injury.Methods : 42 adult, male, Sprague-Dawley rats were administered intraperitoneal injections of paraquat (35 mg/kg body weight). SP-A and SP-D levels were determined via Western blot. LPO in the left lung homogenate was measured via analyses of the levels of thiobarbituric acid-reactive substances.Results : LPO levels peaked at 6 hours, with no associated histological changes. SP-D levels increased until hour 12 and declined until hour 48; SP-D levels subsequently began to increase again, peaking at hour 72. SP-A levels peaked at hour 6, declining thereafter.Conclusions : We suggest that in the early phase of paraquat injury, SP-D levels reflect alveolar damage and that de novo synthesis of SP-D takes 72 hours. Levels of SP-A, on the other hand, reflect abnormalities in the surfactant system in the late stage of paraquat intoxication. Surfactant proteins may play a role in protecting the lungs from reactive oxygen injury. A time-dependent variation has been observed in the levels of surfactant proteins A and D following paraquat injury, and it has been suggested that these proteins play a role in the protection of lung tissue against ROS-induced injuries.
It is difficult to distinguish a lung cancer from a pulmonary tuberculoma or other benign nodule. It is even more difficult to identify the type of lesion if the mass shows no change in size or demonstrates slow growth. Only a pathological confirmation can possibly reveal the nature of the lesion. A 61-year-old-woman was referred for a solitary pulmonary nodule. The nodule showed no change in size for the first two years and continued to grow slowly. Pathological and immunological analyses were conducted for confirmation of the nodule. The nodule was identified as a well-differentiated primary pulmonary adenocarcinoma. An LULobectomy was performed, and the post surgical stage of the nodule was IIIA (T2N2M0). Even though there are few risk factors, there is still the possibility of a malignancy in cases of non-growing or slow growing solitary pulmonary nodules. Therefore, pathological confirmation is encouraged to obtain a firm diagnosis.
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