title: Phospholipid alterations elicited by hexachlorobenzene in rat brain are strain-dependent and porphyria-independent.
abstract: Hexachlorobenzene (HCB) alters phospholipid and heme metabolisms in the liver and Harderian gland. The effects of HCB on phospholipid metabolism, in an organ considered to be non-responsive to its porphyrinogenic effects, remain to be studied. Therefore, as the brain is an organ with this feature, this paper analyzes the effects of HCB on brain phospholipid composition in order to investigate if there is any relationship between HCB-induced porphyrin metabolism disruption and phospholipid alterations. For this purpose, a time-course study of HCB effects on brain phospholipids was performed in two strains of rats differing in their susceptibility to acquire hepatic porphyria: Chbb THOM (low); and Wistar (high). This paper shows for the first time that rat brain phospholipids are affected by HCB exposure. Comparative studies show that HCB-induced disturbances in brain phospholipid patterns are time and strain-dependent. Thus, whereas major phospholipids, phosphatidylcholine and phosphatidylethanolamine were more altered in Wistar rats, minor phospholipids, phosphatidylinositol and phosphatidylserine were more affected in Chbb THOM rats. HCB intoxication led to a sphingomyelin/phosphatidylcholine molar ratio lower than the normal, in both strains. As was expected, brain porphyrin content was not altered by HCB intoxication in either strain. It can be concluded that HCB is able to alter brain phospholipid metabolism in a strain-dependent fashion, and in the absence of alterations in brain heme metabolism. In addition, HCB-induced disturbances in brain phospholipids were not related to the degree of hepatic porphyria achieved by the rats.
authors.affiliation: Laboratorio de Porfirias Experimentales y Metabolismo del Hemo, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Nuñez, 1428, Buenos Aires, Argentina.
authors.forename: A C
authors.initials: AC
authors.lastname: Cochón
authors.forename: L C
authors.initials: LC
authors.lastname: San Martín de Viale
authors.forename: S C
authors.initials: SC
authors.lastname: Billi de Catabbi
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006581:Hexachlorobenzene / Q000494:pharmacology*; D009929:Organ Size / Q000187:drug effects; D010713:Phosphatidylcholines / Q000378:metabolism; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010716:Phosphatidylinositols / Q000819:agonists / Q000037:antagonists & inhibitors; D010718:Phosphatidylserines / Q000037:antagonists & inhibitors; D010743:Phospholipids / Q000378:metabolism*; D011164:Porphyrias / Q000378:metabolism; D011166:Porphyrins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013045:Species Specificity; D013109:Sphingomyelins / Q000037:antagonists & inhibitors*
chemical_list: D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D010716:Phosphatidylinositols; D010718:Phosphatidylserines; D010743:Phospholipids; D011166:Porphyrins; D013109:Sphingomyelins; D006581:Hexachlorobenzene