Lung cancer formation is a multifactorial process. Lipid peroxidation is one of oxidative conversion of polyunsaturated fatty acids to products known as malondialdehyde (MDA) or lipid peroxides. However, there is limited information available for a systemic examination of lipid peroxidation, prostaglandin production and Bcl-2 in human lung cancer.
The present study was to measure the lipid peroxidation in human lung cancer and to analyze how lipid peroxidation was associated the prostaglandin production and Bcl-2 expression. Fifty-two non-small cell lung carcinoma (NSCLC) tissue samples and their corresponding non-cancer tissue samples were used in this study.
The level of MDA was significantly increased in the lung cancer tissues, compared with non-cancer lung tissues. Of two prostaglandins measured, thromboxane B2 (TXB2) was much higher in the cancer tissues than non-cancer tissues. Though prostaglandin E2 (PGE2) showed no significant difference. The changes in both TXB2 and PGE2 were not related to cigarette smoking in cases we studied. The expression of Bcl-2, which is also functioned as an antioxidant agent, was significantly elevated in the tumor tissues, compared to the non-tumor tissues. There was a positive correlation between MDA and TXB2 in both cancer and non-cancer lung tissues. MDA level was correlated with Bcl-2 in lung cancer tissues of Stages I and II but was not with those of Stage III. The cancer at the advanced stage appeared to have a higher level of TXB2.
An increase in the lipid peroxidation may be regarded as an oxidant insult and also a marker for high-turn over of TXB2. In conclusion, our study demonstrated that the production of TXB2 was increased in lung caner tissue and that such an increase can result in lipid peroxidation which may be met by an elevation in Bcl-2 expression.
Our study suggests that the level of lipid peroxidation, thromboxane and Bcl-2 may serve as a marker for assessing the stage of the tumor and also monitoring the potential metastasis.
George Chen, None.