Histochemical studies of artemether, fuvinazole and niridazole on schistosomula of Schistosoma japonicum and mouse livers1
Abstract
Artemether 300 mg/kg, fuvinazole 400 mg/kg and niridazole 200 mg/kg were given ig for 2d to mice infected 7 d previously with 500-1000 cercariae. Histochemical observations were made 8, 9, 11 and 15 d after infection.
The glycogen content of schistosomula decreased markedly 1-7 d after niridazole and artemether, and reduced gradually after fuvinazole, but increased in the untreated controls.
The alkaline phosphatase (AKP) in 8 d to 15 d old schistosomula were distributed in the tegument and parenchymal cells. After medication, the AKP in worm tegument was significantly inhibited by fuvinazole, while that in the parenchymal cells was inhibited by artemether and niridazole.
The glycogen content and the AKP activity in the liver tissue surrounding the periportal vein obstructed by schistosomula also decreased or even disappeared. It is possible that the hepatic focal anemia caused by dead schistosomula is the main cause of the histochemical changes mentioned above. Severe hepatic damages were seen in the niridazole group.
Keywords:
The glycogen content of schistosomula decreased markedly 1-7 d after niridazole and artemether, and reduced gradually after fuvinazole, but increased in the untreated controls.
The alkaline phosphatase (AKP) in 8 d to 15 d old schistosomula were distributed in the tegument and parenchymal cells. After medication, the AKP in worm tegument was significantly inhibited by fuvinazole, while that in the parenchymal cells was inhibited by artemether and niridazole.
The glycogen content and the AKP activity in the liver tissue surrounding the periportal vein obstructed by schistosomula also decreased or even disappeared. It is possible that the hepatic focal anemia caused by dead schistosomula is the main cause of the histochemical changes mentioned above. Severe hepatic damages were seen in the niridazole group.