Serum Glutamic Oxaloacetic Transaminase Levels Research Articles

In vivo prevention of cyclophosphamide-induced Ca 2+ dependent damage of rat heart and liver mitochondria by cyclosporin A

The use of Cyclophosphamide, an anti-cancer and immunosuppressant drug, is accompanied by a number of side effects. Rats injected with a single dose of cyclophosphamide (200 mg kg −1 body weight) showed an increase in the levels of serum glutamate-oxaloacetate transaminase, serum glutamate-pyruvate transaminase, glucose-6-phosphate dehydrogenase and creatine phosphokinase isoenzyme by 53, 24, 55 and 135%, respectively. Also the ability of heart or liver mitochondria to retain accumulated Ca 2+ and tetraphenylphosphonium ion was sharply affected in treated rats. Rats injected with the same dose of cyclophosphamide plus cyclosporin A (500 μg kg −1 body weight) showed reduction in the levels of those enzymes by about 44, 21, 43 and 57%, respectively compared to cyclophosphamide-treated rats. Cyclosporin A treatment also restored mitochondrial ability to retain accumulated Ca 2+ and tetraphenyl phosphonium ions nearly to the level of untreated rats. We suggest that cyclophosphamide induced cardio and hepatotoxicity by increasing heart and liver inner mitochondrial membrane permeability to Ca 2+. The protective effect of cyclosporin A against cyclophosphamide-induced damage also support this suggestion.

Altered hepatic hemodynamics and improved liver function following intrahepatic vascular infusion of prostaglandin E1.

Prostaglandin E1 (PGE1) has cytoprotective effects in the liver. To find how PGE1 influenced hepatic hemodynamics, oxygen metabolism, and hepatic function, we carried out an experimental and a clinical study. PGE1 was continuously administered into the hepatic artery (n = 5) or portal vein (n = 5) at a rate of 0.01 micrograms/kg per min in healthy mongrel dogs. In the clinical study, in eight patients PGE1 was administered through the hepatic artery at a rate of 0.01 micrograms/kg per min after hepatic lobectomy. In the experimental study, hepatic hemodynamics and oxygen metabolism did not change during the administration of PGE1 into the portal vein. During administration of PGE1 into the hepatic artery, hepatic arterial flow increased 1.5-fold after administration compared to the rate before administration (P < 0.01). Hepatic arterial pressure, hepatic arterial resistance, and post-sinusoidal resistance significantly decreased after administration (P < 0.01, P < 0.01, and P < 0.05, respectively). Hepatic oxygen supply increased significantly (P < 0.01). In the patients, serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels remained low after surgery, and the recovery of protein synthesis was improved compared with that in eight hepatectomized patients without PGE1 administration (controls). The intrahepatic arterial infusion of PGE1 was considered useful for the recovery of liver function.

Continuous hepatocyte growth factor supply prevents lipopolysaccharide-induced liver injury in rats

We present a rat model in which continuous supply of hepatocyte growth factor (HGF) prevents liver injury induced by carbon tetrachloride (CCl 4) and E. coli 011:B4 lipopolysaccharide (LPS). Rat fibroblasts genetically modified to secrete rat HGF were implanted in syngenic rat spleen 7 days before administration of the hepatotoxins. Rats with HGF-secreting fibroblasts in the spleen showed a dramatic resistance to CCl 4- and LPS-induced liver injury. In the LPS-induced liver injury model, blood chemical analysis revealed that the increase in serum glutamic oxalacetic transaminase level and the decrease in blood sugar level were remarkably suppressed in rats with HGF-secreting cells in the spleen. Most importantly, their survival rate was greatly improved compared to other control groups of rats. Thus our results indicate a new role of HGF in liver protection during endotoxemia and convey important clinical implications for developing new therapeutic modalities in the treatment of liver failure caused by endotoxemia.

Role of Exogenousl-Arginine in Hepatic Ischemia–Reperfusion Injury

Plasmal-arginine is usually deficient immediately after hepatic reperfusion in orthotopic liver transplantation, which may also contribute to the occurrence of either hepatic ischemia–reperfusion injury or pulmonary hypertension. In this study, exogenousl-arginine was thus experimentally used to reverse the deficient status of thel-arginine/NO pathway. Anin vivomodel of 1 hr hepatic ischemia and reperfusion was thus tested in both rats (Experiment A) and pigs (Experiment B). In Experiment A, 10 mg/kg ofl-arginine (group 1,n= 7),d-arginine (group 2,n= 7), or saline (group 3,n= 7) was administered through the portal vein. The hepatic tissue blood flow, at 20 min after reperfusion, improved in group 1 (70.7 ± 7.0% of the preclamp levels) compared to groups 2 and 3. The serum glutamate oxaloacetate transaminase levels at 24 hr after reperfusion were also lower in group 1 (320 ± 22.2 IU/L) than in either group 2 or group 3. The intrahepatic NO levels showed a temporal burst (>15,000 pA current) after reperfusion only in group 1. In Experiment B, 10 mg/kg ofl-arginine (group 4,n= 5),d-arginine (group 5,n= 5), or 10 ml of saline (group 6, n = 5) was administered through the portal vein. In group 4, the MPAP (mean pulmonary arterial pressure)/MAP (mean arterial pressure) was lower than that observed in groups 5 and 6. In conclusion, exogenousl-arginine administered from the portal vein was thus found to be effective in mitigating both portal hypertension and reperfusion injury by producing an increased amount of NO immediately after reperfusion.

Protective and Therapeutic Effect of the Indonesian Medicinal HerbCurcuma xanthorrhizaon β-D-Galactosamine-induced Liver Damage

The present study was carried out to investigate the hepatoprotective effects of a dose of C. xanthorrhiza on acute hepatotoxicity induced in rats by a single dose of β-D-galactosamine (288 mg/kg, i.p.), and its mechanism of action. C. xanthorrhiza (100 mg/kg) was administered p.o. to experimental animals according to the protocol followed by the i.p. administration of a single dose of hepatotoxin. Hepatoprotective activity was monitored by estimating serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) levels and histopathological changes in the livers of C. xanthorrhiza -treated and untreated groups of animals. The results clearly indicated that the extract of C. xanthorrhiza significantly reduced the acute elevation of serum transaminases induced by hepatotoxin, and alleviated the degree of liver damage at 24 h after the intraperitoneal administration of the hepatotoxins.

Protective and therapeutic effects of huanglian-jie-du-tang on hepatotoxin-induced liver injuries.

The hepatoprotective effect of Huanglian-Jie-Du-Tang (HLJDT), a Chinese medicinal prescription, was investigated in three kinds of experimental models. The animals were treated with HLJDT (300 mg/kg, p.o.) thrice at 2, 4 and 10 hours after administration with carbon tetrachloride (32 microliters/kg, i.p.), acetaminophen (600 mg/kg, i.p.) and beta-D-galactosamine (188 mg/kg, i.p.). Significant hepatoprotective effects on carbon tetrachloride and acetaminophen induced liver injuries were noted, but no significant effect on beta-D-galactosamine induced liver injury was observed. These hepatoprotective effects were evidenced by comparing the serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) levels in HLJDT treated and untreated groups. Serum enzyme activities in the carbon tetrachloride and acetaminophen experiments were significantly lower in the treated groups while the herbal prescription has no effect on the beta-D-galactosamine experiment. These results demonstrated that Huanglian-Jie-Du-Tang has a hepatoprotective effect against experimental liver injuries induced by specific hepatotoxins, and therefore may be useful in treating some, but not all, liver injuries.

Toxicity study of hepatic artery infusion chemotherapy with massive dose FUDR in rats

Hepatic artery infusion (HAI) of fluoroudeoxyuridine (FUDR) has been shown to be effective in the treatment of liver metastases from colorectal cancer. However, local toxicity is the most serious limitation of this therapy. The aetiology of HAI toxicity remains unclear. To assess the HAI toxicity, forty-eight non-tumour-bearing, healthy BD-IX rats were randomized to control or treatment groups. The control group (n = 24) received heparinized saline alone (200 u heparin kg-1 day-1) and the treatment group (n = 24) received 6.7 mg FUDR kg-1 day-1 (equivalent to the human dose of 1.0 kg-1 day-1) via HAI for 28 days. Blood samples were collected for haematologic and biochemical analysis twice a week (on days 3 and 7). Toxicity was evaluated by determination of mortality, body weight, white blood cell (WBC) count, serum glutamic oxaloacetic transaminase (SGOT), alkaline phosphatase (ALP), total bilirubin and blood urea nitrogen (BUN), and creatinine. No significant differences in WBC, SGOT, BUN and creatinine levels were found between the group receiving FUDR treatment and the control group. Significantly higher total bilirubin levels, mortality and body weight loss were found in the FUDR-treated group than in the control group. A multivariate analysis revealed that total bilirubin level was the only significant predictor of mortality in the FUDR treatment group. These results suggested that biliary tract damage seems to be the principal toxicity of HAI FUDR chemotherapy.

The protective effects of eugenol on carbon tetrachloride induced hepatotoxicity in rats.

Our earlier studies in vitro have shown that eugenol inhibits liver microsomal monooxygenase activities and carbon tetrachloride (CCl4)-induced lipid peroxidation (Free Rad. Res. 20, 253-266, 1994). The objective of the present investigation was to study the in vivo protective effect of eugenol against CCl4 toxicity. Eugenol (5 or 25 mg/kg body wt) given orally for 3 consecutive days did not alter the levels of serum glutamic oxalacetic transaminase (SGOT), microsomal enzymes such as cytochrome P450 reductase, glucose-6-phosphatase (G-6-Pase) xenobiotic-metabolizing enzymes (aminopyrine-N-demethylase, N-nitrosodimethylamine-demethylase and ethoxyresorufin-O-deethylase) and liver histology. Doses of eugenol (5 or 25 mg/kg) administered intragastrically to each rat on three consecutive days i.e. 48 hr, 24 hr and 30 min before a single oral dose of CCl4 (2.5 ml/kg body wt) prevented the rise in SGOT level without appreciable improvement in morphological changes in liver. Eugenol pretreatment also did not influence the decrease in microsomal cytochrome P450 content, G-6-Pase and xenobiotic-metabolizing enzymes brought about by CCl4. Since eugenol is metabolized and cleared rapidly from the body, the dose schedule was modified in another experiment. Eugenol (0.2, 1.0, 5.0 or 25 mg/kg) when given thrice orally i.e. prior to (-1 hr) along with (0 hr) and after (+3 hr) the i.p. administration of CCl4 (0.4 ml/kg) prevented significantly the rise in SGOT activity as well as liver necrosis. The protective effect was more evident at 1 mg and 5 mg eugenol doses. However, the decrease in microsomal G-6-Pase activity by CCl4 treatment was not prevented by eugenol suggesting that the damage to endoplasmic reticulum is not protected. The protective effect of eugenol against CCl4 induced hepatotoxicity is more evident when it is given concurrently or soon after rather than much before CCl4 treatment.

Effects of saikosaponins on hepatic damage induced by halothane and hypoxia in phenobarbital-pretreated rats.

The effects of saikosaponins-a.-b1,-b2,-c, and-d on hepatic damage induced by halothane and hypoxia were investigated in the rat. Inhalation of halothane under a hypoxic condition significantly increased serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels in rats pretreated with phenobarbital compared with rats pretreated without phenobarbital. Pretreatment with saikosaponin (especially-a and-d) and with phenobarbital suppressed the increase in serum GOT and GPT levels in comparison with the rats treated with phenobarbital, halothane, and hypoxia. Histological observation also confirmed that pretreatment with saikosaponin had a protective effect against liver cell damage caused by halothane and hypoxia. Saikosaponins-a and-d, the most effective saikosaponins against hepatic damage, inhibited the increases in cytochrome P450 and NADPH-cytochromec reductase activity which are induced by phenobarbital treatment. Therefore, it is suggested that the cytoprotective effect of saikosaponin against halothane-induced hepatitis under hypoxia is caused by inhibition of phenobarbital stimulation of the enzyme system for hepatic drug metabolism.

CHEST TRAUMA: Assessment, Diagnosis, and Management

The aim of this study was to evaluate the hypoglycemic, hypolipidemic, and anti-inflammatory potentials of ethanolic extract of leaves of Amaranthus paniculatus linn. (EEAP) on alloxan-induced diabetic rats scientifically. Hyperglycemia induces the generation of free radicals which can affect antioxidant defenses, thus leading to the disruption of beta cellular functions, oxidative damage to membranes, leading to the release of C-reactive protein and altered lipid metabolism.Diabetes was induced by intraperitoneal injection of ice-cold aqueous alloxan monohydrate at the dose of 150 mg/kg body weight.After a daily single oral administration of the EEAP for 28 days starting from the study protocol, the blood glucose, serum glutamic pyruvic transaminase (SGPT), serum glutamic oxaloacetic transaminase (SGOT), total cholesterol (TC), triglyceride (TG), and C-reactive protein (CRP) levels were assessed. The results obtained from the study administration of daily dose of EEAP significantly reduced the blood glucose, SGPT, SGOT, TC, TG, and CRP in a dose-dependent manner. The results obtained were comparable to those of glibenclamide. The serum levels of TC, TG, and CRP were significantly altered in the diabetic control group, but it was significantly decreased in the extract-treated group and standard glibenclamide-treated group, except at a dose of 100 mg/kg where there was no significant effect on the TG level. The finding obtained suggests that EEAP acts through molecular level, modifying the altered pathways in diabetes and associated complications.The results obtained suggest that EEAP possesses a potential for the management of diabetes and associated complications in experimentally-induced diabetic rats.

Frequency and prognosis of stroke/TIA among 4808 survivors of acute myocardial infarction. The SPRINT Study Group.

Stroke complicating acute myocardial infarction is associated with substantial morbidity and mortality. The purpose of this study was to assess the incidence, predictors, and impact on mortality of stroke/transient ischemic attacks occurring after hospital discharge in a large unselected population of acute myocardial infarction survivors. During a secondary prevention study with nifedipine (SPRINT), demographic, anamnestic, and clinical data were collected for 5839 consecutive acute myocardial infarction patients admitted to 13 coronary care units in Israel. Hospital survivors (n = 4808) were followed for a year after their discharge. Mortality was assessed for a mean follow-up of 5.5 years (range, 4.5 to 7 years). One percent (48/4808) of hospital survivors from acute myocardial infarction experienced a stroke/transient ischemic attack in the year after acute myocardial infarction. Thirty-one percent (15 of 48) of events occurred in the first month after hospital discharge. Incidence was higher among older patients (> 70 years; 1.9%), those with anterior site of myocardial infarction (1.35%), a previous history of myocardial infarction (1.8%), hypertension (1.4%), stroke in the past (4.1%), and chronic atrial fibrillation (9%). Multivariate analysis identified the following as independent predictors of stroke/transient ischemic attacks occurring in the year after hospital discharge: chronic atrial fibrillation, older age, history of previous myocardial infarction, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, and stroke in the past. The age-adjusted 1-year and long-term mortality rates (4.5 to 7 years; mean, 5.5 years) were significantly higher in patients with (31% and 62%) than in those without stroke/transient ischemic attacks (9% and 31%, respectively; P < .01). Stroke/transient ischemic attack is a relatively rare (1%) complication in the year after hospital discharge from acute myocardial infarction, though more frequent in the first month. Chronic atrial fibrillation, older age, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, past myocardial infarction, and stroke identify high-risk patients. Patients suffering from subsequent stroke/transient ischemic attacks experienced higher mortality than counterparts who remained free from this complication.

Experimental murine protoporphyria induced by griseofulvin (GF): the relationship between hepatic porphyrin levels and liver function test values in mice treated with GF.

To investigate the hepatic abnormalities accompanying experimental protoporphyria due to griseofulvin (GF), liver function test values and porphyrin levels in mice were assayed at days 2, 4, 8, and 16 after starting the administration of 0.5% GF feed. Furthermore, in an attempt to elucidate the harmful effects of GF on liver functions, the above mentioned assay was also performed after the feed was discontinued in mice given 0.5% GF feed for 16 days. The hepatic protoporphyrin (PP) level had already risen by day 2, but the erythrocytic PP level was within normal limits at that time. Hepatic PP levels increased gradually, followed by an increase in erythrocytic PP levels. The variation in liver function test values roughly paralleled the porphyrin levels. Over the time span of the response to GF, the variations in the serum glutamate oxaloacetate transaminase (S-GOT) levels, serum glutamate pyruvate transaminase (S-GPT) levels, and leucine amino peptidase (LAP) levels resembled those in hepatic PP. On the other hand, the changes in alkaline phosphatase (ALP) levels paralleled those of the erythrocytic PP levels. Erythrocytic and fecal protoporphyrin levels decreased to the normal level one month after the discontinuation of GF administration, but the hepatic protoporphyrin level still was 53.6 times higher than the normal level two months after switching to normal feed. The values of liver function tests had returned to within the normal range after one month. By the fourth day after the administration of GF, a brown pigmented material could be observed around the hepatocytes and the Glisson sheath; the amount of this material increased day by day.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in transaminase before and after tonsillectomy

Almost all patients who undergo palatine tonsillectomy for chronic tonsillitis and/or tonsillar hypertrophy manifest postoperative changes in their condition and laboratory data. In some patients, high preoperative transaminase levels decrease postoperatively. I studied 17 patients who had abnormal serum transaminase levels 10 days before tonsillectomy. Before tonsillectomy, serum glutamate oxaloacetate transaminase (GOT) levels were abnormal in half and serum glutamate pyruvate transaminase (GPT) were abnormal in all. Before operation, laboratory values of serum GPT were higher than those of serum GOT in all 17 patients. After tonsillectomy, the abnormal GOT levels in all patients gradually improved to the normal range before the 11th postoperative day and GPT levels did so before the 25th day. Measurement of intracellular transaminase activity of the palatine tonsil suggested that the migration of intracellular transaminase from tonsillar cells to serum would not elevate the serum transaminase level. Postoperative changes in serum transaminase and serum cholinesterase were different from the recovery process observed in fatty liver. The high transaminase level observed in patients with tonsillectomy is suspected to be due to other organs, rather than continuous inflammation of the palatine tonsil.

Periportal high intensity on T2-weighted MR images in acute viral hepatitis.

The frequency and degree of periportal high intensity (PHI) on T2-weighted images in 28 patients (32 MR studies) with acute viral hepatitis were analyzed with regard to the various levels of serum glutamic-oxaloacetic transaminase (SGOT) and clinical phases. Periportal high intensity was found in 16 of 32 MR studies (50%) and no definite PHI was found in 7 studies (22%). Periportal high intensity appeared when the SGOT level was greater than 500 IU or when the phase of the disease was early. Follow-up studies revealed that PHI decreased during clinical recovery. We conclude that the degree of PHI on T2-weighted images reflects the severity of the disease in acute viral hepatitis.

Anti-Hepatitic Activity of Ginesenoside Ro1

Ginsenoside Ro, an oleanane-type saponin has been screened for activity in experimental models of acute and chronic hepatitis. Ginsenoside Ro (50 and 200 mg/kg, P.O.) inhibited the increase of serum glutamic oxaloacetic transaminase (s-GOT) and serum glutamic pyruvic transaminase (s-GPT) levels in D-galactosamine (GalN)- and carbon tetrachloride (CCl (4))-induced acute hepatitic rats. Ginsenoside Ro inhibited the increase of connective tissue in the liver of CCl (4)-induced chronic hepatitic rats. Ginsenoside Ro showed a stronger inhibitory effect on the GalN-induced acute hepatitic model than those of the aglycone of ginsenoside Ro, oleanolic acid, or glycyrrhizic acid and its aglycone, glycyrrhetinic acid.

Effects of Long-Acting Superoxide Dismutase on Liver Metabolism after Major Hepatic Resection in Rats with Cirrhosis

The aim of this study is to clarify the liver metabolic changes after major hepatic resection. The survival rate after 70% hepatectomy of rats with cirrhosis was significantly depressed compared with that of the control group. Mitochondrial function in the cirrhotic liver was disturbed compared with the control group. Tissue levels of hypoxanthine and xanthine increased both in the cirrhotic group and the control group. The increase in xanthine levels was remarkable and was prolonged in the cirrhotic group compared with the control group. Decreases in adenine nucleotides were observed after resection both in normal and cirrhotic livers. These were remarkable and were prolonged in rats with cirrhosis. Administration of polyoxyethylene-modified superoxide dismutase improved the survival rate and lessened decreases in adenine nucleotide levels. Moreover, it accelerated the recoveries of serum glutamic oxaloacetic and pyruvic transaminase levels after resection in rats with cirrhosis. These results indicate that disturbances in energy metabolism and increases in oxygen free radical formation are more remarkable in the cirrhotic liver than in the normal liver, which contributes to a low survival rate in rats with cirrhosis.

Aspirin, hydroxychloroquine, and hepatic enzyme abnormalities with methotrexate in rheumatoid arthritis

Levels of serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) in patients with rheumatoid arthritis from 5 centers involved in the Arthritis, Rheumatism, and Aging Medical Information System were correlated with the use of specific antirheumatic medications. Elevated levels of SGOT and SGPT were most frequent in patients taking salicylates and methotrexate (MTX) and least frequent in patients taking hydroxychloroquine. The combination of MTX and salicylates greatly increased the frequency of abnormal liver enzyme values. In contrast, the addition of hydroxychloroquine to a regimen of either MTX or aspirin essentially eliminated the SGOT and SGPT abnormalities. Results from all 5 centers were consistent and remained so after adjustment for age, sex, and disease duration. Knowledge of these important drug interactions may permit continuation of MTX therapy in patients in whom the drug might otherwise be discontinued.

Postgastrectomy prescription of mitomycin C and UFT for patients with stage IV gastric carcinoma

E arly detection of gastric cancer by upper gastrointestinal series, endoscopy, operative techniques of extensive lymph node dissection, and postoperative chemotherapy has led to improved survival rates. However, a large number of patients with stage IV gastric cancer undergo surgery for purposes of palliation, and the 5-year survival rate remains around 10% [1]. In one study, chemotherapy with mitomycin C and long-term continuous administration of 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur) in the early postoperative period was found to improve the 5-year survival rate for patients with stage III or IV gastric carcinoma [2], whereas in another study, no such effect was noted for stage IV patients [3]. UFT, a combination of tegafur and uracil in a molar ratio of 1:4, was developed as an antitumor drug by Fujii et al [4]. Both animal studies and clinical trials [5] revealed higher levels of 5-fluorouracil (5-FU) in the blood and in tumor tissues in cases with UFT, compared with findings with tegafur or 5-FU. Using an in oivo chemosensitivity test, we found UFT to be more effective than 5-FU and its analogues for treating patients with gastric cancer [6,7]. We report herein the effects of mitomycin C plus UFT as postoperative therapy for gastrectomized patients with stage IV gastric cancer. All 54 patients included in this trial had stage IV gastric cancer and had undergone gastric resection. These patients, who were treated from April 1983 to February 1985, were randomly assigned to either regimen A or B. Regimen A consisted of mitomycin C, 20-mg intravenous injection on the day of operation and 10 mg on day 1 after surgery, and tegafur, 600 mg by mouth daily for 2 years starting 2 weeks after the operation, whereas that of regimen B was mitomycin C in the same dose as that of regimen A, and UFT, 600 mg by mouth daily for 2 years. Patients selected for the study had to have the following: (1) a histologic diagnosis of gastric cancer; (2) a macroscopic diagnosis of a stage IV tumor upon completion of the surgical procedure; (3) age under 76 years; (4) no evident synchronous or metachronous double cancer; and (5) adequate organ system function (leukocyte count greater than 4,000/mm 3, platelet count greater than 100,000/ram 3, serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase levels less than 100 U, and protein-negative urine). Fur-

Seroepidemiology of hepatitis B virus, hepatitis D virus, and human immunodeficiency virus infections among parenteral drug abusers in southern Taiwan.

A total of 390 parenteral drug abusers (PDAs) at the Kaohsiung Municipal Narcotics Abstention Institute were examined for markers of hepatitis B virus (HBV), hepatitis D virus (HDV), and human immunodeficiency virus (HIV). All sera were tested for hepatitis B surface antigen (HBsAg), surface antibody (anti-HBs), and core antibody (anti-HBc) by radioimmunoassay (RIA) and for antibody to HIV (anti-HIV) by enzyme-linked immunosorbent assay (ELISA). Hepatitis B e antigen (HBeAg) and antibody to HDV (anti-HDV) were also tested for HBsAg-positive serum samples. Although the HBsAg-positive rate (22.1%) among PDAs was similar to that of the general population in southern Taiwan, the HBV infection rate (99.2%) and the anti-HDV-positive rate (78.5%) among HBsAg-positive subjects were significantly higher than those of the general population in southern Taiwan (P less than 0.0001). None of the PDAs studied were positive for anti-HIV. The levels of serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) among PDAs were significantly higher than those of the general population in southern Taiwan (P less than 0.0001). The more frequent the institutionalisation, the higher the infection rates with HBV and HDV and elevated levels of SGOT and SGPT. Horizontal transmission through parenteral drug abuse may be considered a possible reason for the significantly higher rates of HBV and HDV among parenteral drug abusers.

Tumor-promoting activity and cytotoxicity of 3,4,3?,4?-tetrachlorobiphenyl on N-nitrosomorpholine-induced murine liver foci

Effects of 3,4,3',4'-tetrachlorobiphenyl (TCB) on glucose-6-phosphatase (G6Pase)-altered hepatic foci of N-nitrosomorpholine (NNM)-treated B6C3F1 mice were investigated. TCB was chosen as a selective 3-methylcholanthrene-type inducer and tumor promoter. To initiate hepatocarcinogenesis, mice were treated with NNM (160 mg/l, in drinking water for 7 weeks), as in previous studies with the rat model. After a treatment-free interval of 22 weeks, TCB was administered (5 x 50 mg/kg, every 3 days), and liver foci were analysed 10 weeks after the start of TCB treatment. Unexpectedly, the number of G6Pase-negative and -positive foci per liver was markedly diminished following TCB treatment (to 32% and 57%, respectively). On the other hand, the mean volume of the remaining G6Pase-altered foci was enhanced, owing to an increase in the percentage of foci of large size (greater than 0.5 mm2). Throughout the experimental period of 39 weeks prolonged liver injury due to NNM and TCB treatment was demonstrated by histology and by elevated serum levels of glutamate-oxaloacetate transaminase. The results suggest that (in contrast to the rat system) TCB exhibited opposing effects on liver foci in the mouse model: (a) moderate tumor-promoting effects and (b) cytotoxic effects in NNM-injured liver, leading to decreased numbers of liver foci.