Free Content Polaprezinc protects gastric mucosal cells from noxious agents through antioxidant properties in vitro

Authors: Hiraishi; Sasai; Oinuma; Shimada; Sugaya; Terano

Source: Alimentary Pharmacology & Therapeutics, Volume 13, Number 2, February 1999 , pp. 261-269(9)

Publisher: Wiley-Blackwell

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Abstract:

Background:

Polaprezinc has been shown to exert an anti-oxidant property in a tube experiment, protect gastric mucosa from experimental ulcerations in vivo, and accelerate the healing of gastric ulcer in humans. Aim:

To examine a possible protective effect of polaprezinc on oxidant-mediated injury in primary monolayer cultures of rat gastric fundic mucosa. Methods:

Cytotoxicity was quantified by measuring 51Cr release. Whether or not polaprezinc exerts an antioxidant property was investigated by determining the effect of this agent on hydrogen peroxide (H2O2)-induced injury. The effects of polaprezinc on superoxide (O2) generation as well as on ethanol (EtOH)-induced injury were also examined. Generation of O2 was assessed by the reduction in cytochrome c. Results:

H2O2 caused a time- and dose-dependent increase in 51Cr release. The dose-response curve of 51Cr release by H2O2 shifted to the right in the presence of polaprezinc. Polaprezinc, at submillimolar concentrations, prevented H2O2-induced 51Cr release. EtOH also caused a dose-dependent increase in 51Cr release, which was prevented by the addition of polaprezinc. The incubation of cells with EtOH caused an increase in cytochrome c reduction, as the concentrations of EtOH increased. Polaprezinc inhibited EtOH-induced cytochrome c reduction. Protection by polaprezinc was microscopically associated with the prevention of monolayer disruption. Conclusions:

Polaprezinc is antioxidative and directly protects gastric mucosal cells from noxious agents through its antioxidant properties in vitro. This finding may provide the theoretical basis for the usage of an antiulcer drug with antioxidant properties for the treatment of gastric inflammation, such as that induced by ethanol.

Document Type: Original article

DOI: http://dx.doi.org/10.1046/j.1365-2036.1999.00458.x

Affiliations: 1: Second Department of Internal Medicine, Dokkyo University School of Medicine, Mibu, Tochigi, Japan

Publication date: 1999-02-01

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