Reference

Effect of D-galactosamine hydrochloride on the pulmonary surfactant in the rat

Effect of D-galactosamine hydrochloride on the pulmonary surfactant in the rat. Suzuki, Yasuhiro; Tabata, Ryoko; Okawa, Kinichi (Fac. Med., Kyoto Univ., Kyoto, Japan). Exp. Mol. Pathol., 28(3), 349-59 (English) 1978. CODEN: EXMPA6. ISSN: 0014-4800. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Administration of D-galactosamine-HCl [1772-03-8] significantly increased the percentage of serum-free cholesterol [57-88-5] and the phospholipid contents of the pulmonary surfactant in the rat. The max. change in the surfactant was obsd. 40 h after treatment with the drug and was preceded by the change in serum cholesterol levels. Larger dosages were needed to cause pulmonary change than to cause the alteration in serum cholesterol levels. Surface activity of the surfactant in treated rats was higher than that in control rats. Free cholesterol increased in the surfactant but this was not accompanied by a change in the lecithin-cholesterol ratio. Fatty acid anal. of lecithin in surfactant revealed the increase in the content of palmitic acid [57-10-3] with a concomitant decrease in myristic acid [544-63-8] and palmitoleic acid [373-49-9] suggesting an increase in dipalmitoyl phosphatidylcholine content. No apparent change was obsd. in alveolar macrophoges. Pulmonary changes induced by this drug may serve as clues to solve the problem of the turnover and the activity of pulmonary surfactant.

D-Galactosamine-induced liver injury in immunosuppressed mice

D-Galactosamine-induced liver injury in immunosuppressed mice. Schaff, Zsuzsa; Lapis, K.; Szendroi, M. (Med. Sch., Semmelweis Univ., Budapest, Hung.). Acta Morphol. Hung., 32(1), 67-72 (English) 1984. CODEN: AMHUDE. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Thymectomized DBA/2 mice, irradiated with 720 rad/min and reconstituted with syngeneic bone marrow, were treated i.p. with 1 g/kg D-galactosamine-HCl (DGA) [1772-03-8]. Light and electron microscopic changes characteristic of the toxic effect of the agent, such as hepatocellular cytoplasmic inclusions and unicellular necrosis, could be obsd. but no inflammatory reaction was detectable in the liver. The phagocytic activity of Kupffer cells was unchanged in immunosuppressed animals. Liver regeneration following DGA injury took place in 120 h exactly as in animals having an intact immune system. Thus, T-lymphocytes participate in the development of DGA-hepatitis and their absence does not influence the restoration of liver injury. The exptl. system described seems to be suitable for sepg. primary and secondary events and also for studying the role of the immune system in toxic liver injury.