Published online Oct 1, 1995. doi: 10.3748/wjg.v1.i1.13
Revised: July 20, 1995
Accepted: September 1, 1995
Published online: October 1, 1995
AIM: To study the metabolic features of gastric cancer cells, the relationship between intestinal metaplasia or dysplasia and gastric cancer, and the relationship between LDH isoenzymes and the biological behavior of gastric cancer.
METHODS: The content and distribution of LDH isoenzymes LDH-5 and LDH-H in 60 cases of gastric cancer were examined by immunohistochemistry and immunoelectron microscopy.
RESULTS: The content of LDH-5 was significantly higher in gastric cancer cells than in chief cells, surface epithelium and pyloric glandular epithelium, but was similar between gastric cancer cells and parietal cells. The content of LDH-H was significantly lower in gastric cancer cells than in parietal cells, but was similar between gastric cancer cells, chief cells and surface epithelium. The product of LDH-5 but not LDH-H was mainly distributed in the cytoplasmic matrix in the cancer cells. The content of LDH-5 in intestinal metaplasia and dysplasia was significantly higher than in the pyloric glandular epithelium, but was similar to the content in gastric cancer cells. The content of LDH-H was significantly higher in intestinal metaplasia and dysplasia than in both the pyloric glandular epithelium and gastric cancer cells.
CONCLUSION: Increased LDH in gastric cancer cells resulted mainly from increased levels of LDH-5. The LDH-5-mediated elevation in lactate levels could decrease the pH, thereby activating acid hydrolase and indirectly promoting the invasion and spread of gastric cancer cells. Intestinal metaplasia and dysplasia might be an intermediate phase between normal gastric mucosa and gastric cancer.