S. Kapicioglu et al., THE INHIBITING EFFECT OF COLA ON GASTRIC-MUCOSAL CELL-CYCLE PROLIFERATION IN HUMANS, Scandinavian journal of gastroenterology, 33(7), 1998, pp. 701-703
Background: Acidic beverages may be involved in regulating the cell pr
oliferation of the gastric mucosa. We therefore analyzed the interacti
on of Coca-Cola consumption and gastric mucosal proliferation by means
of flow cytometry. Methods: Sixteen healthy students agreed to partic
ipate in this study. All volunteers underwent an oesophagogastroduoden
oscopy after a 12-h overnight fas:. Endoscopic changes in the gastric
mucosa were determined quantitatively. One day later, after a 12-h ove
rnight fast, all volunteers received standard Coca-Cola (200 ml, pH 2.
6, 4 degrees C). One hour later all volunteers again underwent oesopha
gogastroduodenoscopy, to measure gastric mucosal damage. During both t
he first and the second endoscopy at least four biopsy specimens were
taken from the antrum for flow cytometric analysis. Results: The endos
copic analysis showed that there was no difference before and after Co
ca-Cola consumption. However, the flow cytometric analysis showed that
Coca-Cola inhibited the proliferation index and the S phase. Before C
oca-Cola consumption G0/G1: 60 (57-62), G2/M: 0.6 (0.2-1), S: 40 (37-4
2). and PI: 0.40 (0.38-0.43) and after Coca-Cola consumption G0/G1: 70
(60-73), G2/M: 1.9 (1.2-2.5), S: 28 (26-32), and PI: 0.30 (0.27-0.34)
the cell population G0/G1 and G2/M phases were significantly increase
d (P < 0.0001, 0.0003), and the cell population S and PI phases were s
ignificantly low compared with the pre-consumption data (P < 0.0002, 0
.0001). Conclusion: The cell cycle analysis reflects that Coca-Cola in
hibits a crucial event in the cell cycle occurring at the G1/S border.