ABSTRACT-Lipid peroxidation was assessed histologically and biochemically in hemoglobin-free perfused rat livers using two different types of stimulators. The Schiff reaction of fuchsin with cellular aldehydes was used as a histological index for lipid peroxidation. t-Butyl hydroperoxide (BHP, 0.8 mM) infusion caused a rapid and sus tained release of thiobarbituric acid reactive substances (TBARS) into the effluent perfusate for up to 60 min, which was accompanied by lactate dehydrogenase (LDH) leakage after 30 min. The Schiff positive foci were initially restricted to periportal zones and spread with time to whole areas, accompanied by periportal necrosis. Co infusion of diphenyl-p-phenylenediamine suppressed the TBARS release, with nega tive fuchsin staining, but the LDH leakage was unaffected. Under retrograde perfu sion, BHP produced pericentral staining and necrosis. With 2.5 mM ADP-100'U M Fe3+, little TBARS was released up to 60 min, even though the hepatic TBARS levels increased considerably by this time. By 90 min, marked TBARS release occurred, but LDH leakage remained low. Irrespective of the direction of perfusion, pericentral hepatocytes became Schiff positive after 30 min. The fuchsin staining method may be useful for detecting peroxidized zones of the liver lobules.

Bromotrichloromethane (CBrC13)-induced hepatic lipid peroxidation and cell necrosis were studied histologically and biochemically, using isolated perfused livers from phenobarbital-pretreated rats. Lipid peroxidation was assessed by fuchsin staining of the liver slices and release of thiobarbituric acid reactive substances (TBARS) into the perfusate; necrosis was assessed by trypan blue uptake and lactate dehydrogenase (LDH) leakage. A good correlation was observed between the Schiff positive reaction and TBARS release under various experimental conditions, support ing the validity of the fuchsin staining method for histological detection of lipid perox idation. Lobular localization of lipid peroxidation and necrosis was as follows: Under high oxygen supply (95% 02-saturated buffer), infusion of CBrC13 caused the Schiff positive reaction in the pericentral to midzonal hepatocytes, irrespective of the direc tion of perfusion, but did not produce necrosis. Under low oxygen supply (20% 02) with retrograde perfusion, dissociation of lipid peroxidation and necrosis was observed, i.e., trypan blue uptake in the periportal zones and Schiff-positive staining in the pericentral hepatocytes. Thus, lipid peroxidation by itself may have a relatively minor role in the development of CBrC13-induced acute hepatic cell death.

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