When halothane was first introduced into the clinical anesthesia in 1956, it was acclaimed as the ideal anesthetic agent. Soon after its clinical introduction, reports were published regarding jaundice and hepatic necrosis following its use. Stock and Strunin group the etiologic factors as biotransformation, hypersensitivity (immune-related), hypoxia and pharmacogenetic. In contrast, Calahan and Mangano list as possible causes hypoxia, trauma, viral hepatitis and toxic injury. A few cases of hepatitis following enflurane anesthesia have been described and a diagnosis of enflurane hepatitis was made. However, it is much rare than halothane hepatitis and the case remains unproven. Regional anesthesia with local anesthetic agent (lidocaine or bupivacaine) does not cause hepatic injury, even patients with moderate hepatocellular disease may well be able to metabolize durgs normally. Decrease in hepatic blood flow in healthy individuals will cause no problems with regional anesthesia, as the blood flow and cardiac output can be reestablished with the use of fluids or appropriate vasoconstrictors. This study was undertaken to evaluate the effects of halothane, enflurane, and regional anesthesia with lidocaine or bupivacaine on liver function, particularly with serum glutamic oxaloacetic and pyruvic transaminases (SGOT and SGPT) values which are the most frequently determined indicators of possible liver disease. Whereas SGOT is present in a variety of tissues, SGPT appears to be the liver-specific transaminase. We studied randomly-selected 219 patients, ASA class I or II, aged 15-68 yr, scheduled for elective surgery. They had no history of liver disease, and preoperative liver function tests were within normal limit. And we excluded blood transfused cases in this study. They were divided into three groups according to the anesthetic agent used; Group I: Halothane anesthesia (116 cases). Group II: Regional anesthesia (50 cases). Group III: Enflurane anesthesia (53 cases). We also divided subgroups according to the duration of anesthesia in each group; Subgroup A (Subg-A): under 2 hours of anesthesia. Subgroup B (Subg-B): more than 2 hours of anesthesia. SGOT and SGPT were measured before surgery, and on 1st, 3rd and 5th postoperatine days. The results we as follows: 1) The values of SGOT and SGPT were increased (p<0.01) in both Subg-A and B of Group I. However, on the 1st post-operative day they were more prominently elevated than the other postoperative days (P<0.05), but clinically the change of values was all within normal limits. 2) The values of SGOT were increased (P<0.05) in Subg-B of Group II on the 3rd postoperatine day hut clinically were within normal limits. The values of SGPT in Group II were slightly increased within normal ranges. 3) The values of SGOT were increased in Subg-A (P<0.05) and Subg-B (P<0.01) of Group III on the 1st postoperatine day, but clinically were within normal limits. The values of SGPT in Group III were slightly increased within normal ranges. 4) In comparing Group I and Group II, the value of SGOT in Group I was significantly increased than Group II (P<0.05), but clinically was within normal limits, and the change in that of SGPT was not significant. 5) In comparing Group II and Group III, the value of SGOT in Group II was significantly increased (P<0.01) on the 5th postoperatine day than Group III, but clinically was within normal limits, and changes of SGPT were not significant. 6) In comparing Group II and Group III, the values of SGOT and SGPT were not significantly different. 7) The results show that the effect of halothane on liver function (SGOT, SGPT) is not significantly different from those of enflurane and regional anesthesia with local anesthetics.