1998•Journal of Toxicologic PathologyOpen access

The Initial Lesions Caused by Sodium Chloride in Canine Gastric Mucosa.

Yasuyuki Misawa, Tetsuro Sugimoto, Shuichi Chiba, Atsuhiko Kato, Tsuneo Ito, Rikio Niki

Open full text 0 citations

Abstract

Etiologic research has shown that sodium chloride contributes to gastric carcinogenecity. We investigated the initial changes of gastric mucosa in the cytoplasmic mucin of superficial epithelium and the surface mucous layer of Beagle dogs after an oral dose of sodium chloride. Animals were sacrificed at 0.5, 1.5, 3.5 and 5.5 hours after dosing with 5 g of sodium chloride filled gelatin capsules. Sodium chloride caused lesions such as degeneration and detachment of epithelium, and erosion of mucosa as early as 0.5 hours after administration. ConA type III mucin, the evidence for the origin from gland mucous cells, increased after treatment and was found to be thick at the area of the lesion with progression of decreased mucin in the surface mucous layer, or where epithelial detachment occurred. Gland mucous cell mucin might be responsible for the protection and healing of gastric epithelium. Sulfomucin, demonstrated by high iron diamine staining, originally in the lower foveolar cells of the gastric pits was widely observed in the superficial epithelium of the luminar surface during the time course of the study. PCNA positive generative cells originally in the ithmus and parietal cells originally below the gastric pits were also found among superficial epithelial cells of the luminar surface. It was suggested that these cells might cover the lesion as well as superficial epithelium next to the detaching part.

Open-access reader

About this research paper

What this paper is about

Etiologic research has shown that sodium chloride contributes to gastric carcinogenecity. We investigated the initial changes of gastric mucosa in the cytoplasmic mucin of superficial epithelium and the surface mucous layer of Beagle dogs after an oral dose of sodium chloride. Animals were sacrificed at 0.5, 1.5, 3.5 and 5.5 hours after dosing with 5 g of sodium chloride filled gelatin capsules. Sodium chloride caused lesions such as degeneration and detachment of epithelium, and erosion of mucosa as early as 0.5 hours after administration. ConA type III mucin, the evidence for the origin from gland mucous cells, increased after treatment and was found to be thick at the area of the lesion with progression of decreased mucin in the surface mucous layer, or where epithelial detachment occurred. Gland mucous cell mucin might be responsible for the protection and healing of gastric epithelium. Sulfomucin, demonstrated by high iron diamine staining, originally in the lower foveolar cells of the gastric pits was widely observed in the superficial epithelium of the luminar surface during the time course of the study. PCNA positive generative cells originally in the ithmus and parietal cells originally below the gastric pits were also found among superficial epithelial cells of the luminar surface. It was suggested that these cells might cover the lesion as well as superficial epithelium next to the detaching part.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Etiologic research has shown that sodium chloride contributes to gastric carcinogenecity. We investigated the initial changes of gastric mucosa in the cytoplasmic mucin of superficial epithelium and the surface mucous layer of Beagle dogs after an oral dose of sodium chloride. Animals were sacrificed at 0.5, 1.5, 3.5 and 5.5 hours after dosing with 5 g of sodium chloride filled gelatin capsules. Sodium chloride caused lesions such as degeneration and detachment of epithelium, and erosion of mucosa as early as 0.5 hours after administration. ConA type III mucin, the evidence for the origin from gland mucous cells, increased after treatment and was found to be thick at the area of the lesion with progression of decreased mucin in the surface mucous layer, or where epithelial detachment occurred. Gland mucous cell mucin might be responsible for the protection and healing of gastric epithelium. Sulfomucin, demonstrated by high iron diamine staining, originally in the lower foveolar cells of the gastric pits was widely observed in the superficial epithelium of the luminar surface during the time course of the study. PCNA positive generative cells originally in the ithmus and parietal cells originally below the gastric pits were also found among superficial epithelial cells of the luminar surface. It was suggested that these cells might cover the lesion as well as superficial epithelium next to the detaching part.

Key concepts: Foveolar cell, Gastric mucosa, Mucin, Epithelium, Pathology, Staining, Beagle, Sodium

Related papers

Back to paper searchBrowse research topicsOriginal source
The Initial Lesions Caused by Sodium Chloride in Canine Gastric Mucosa. — Research Paper | ScholarLens