Maintaining abstinence from alcohol with gamma-hydroxybutyric acid.
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Publications and source records attributed to G Gasbarrini.
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While cerebral atrophy has been shown in patients with anorexia nervosa, cerebellar atrophy has never been reported in these patients. We report a case of cerebral atrophy with marked cerebellar atrophy in a 20-year-old woman with anorexia nervosa admitted to our hospital for severe weight loss. Neuroradiological examinations of the patient showed morphological brain alteration without focal parenchymal lesions. Cranial computerized tomography (CCT) showed an enlargement of the external cerebrospinal fluid spaces, especially those close to the cerebellar cistern. A brain magnetic resonance imaging (MRI) study confirmed the results of the CCT and dynamic single-photon emission tomography (d-SPECT) showed a reduced perfusion of the left brain areas. The reported case shows that some forms of anorexia nervosa have a concomitant presence of cerebral and cerebellar morphological anomalies. At present, it is not possible to demonstrate the whole correlation between the imaging reports and the clinical or neurological symptomatology. Some forms of brain alteration could be secondary to undernutrition; on the other hand, cerebral and cerebellar atrophy and eating disorders are far from clear and may also be an expression of an unknown common denominator.
Twenty-four-hour energy expenditure (EE) and substrate oxidation (respiratory chamber), and whole-body glucose uptake and oxidation rates (euglycemic hyperinsulinemic clamp [EHC] and indirect calorimetry) were measured in 10 male patients with posthepatitis, Child B cirrhosis, and 8 healthy male controls matched for age, body size, and body composition. Twenty-four-hour EE was higher in cirrhotic patients than in controls (8,567 +/- 764 vs. 6,825 +/- 507 kJ/d; P < .001). Resting energy expenditure (REE) was also higher in cirrhotic patients than in controls (7,881 +/- 1,125 vs. 5,868 +/- 489 kJ/d; P < .01). Twenty-four-hour respiratory quotient (RQ) (trend) and fasting RQ (0.76 +/- 0.05 vs. 0.82 +/- 0.04; P < .05) were lower in cirrhotic patients than in controls, reflecting higher lipid oxidation rates in the former group. Whole-body glucose uptake was markedly reduced in cirrhotic patients when compared with controls (22.4 +/- 3.2 vs. 44.5 +/- 7.6 mmol/kg/min; P < .001). Carbohydrate oxidation rates, computed during the last 40 minutes of the clamp, were 8.5 +/- 1.1 mmol/kg/min in cirrhotic patients and 22.6 +/- 6.1 mmol/kg/min in controls (P < .001). Nonoxidative glucose disposal was 13.9 +/- 2.5 mmol/kg/min in cirrhotic patients and 22.0 +/- 5.5 mmol/kg/min in normal controls (P < .01). In conclusion, our data indicate that patients with Child B cirrhosis who still maintain a nutritional status (i.e., body composition) comparable with healthy controls are characterized by a cluster of metabolic defects that include hypermetabolism, increased lipid utilization, and insulin resistance. This suggests that the above metabolic syndrome precedes and probably leads to malnutrition in the natural history of the liver disease. In fact, in spite of the absence of a significant difference in caloric intake between cirrhotic patients and normal controls, the elevated 24-hour EE might allow for a relevant weight loss in cirrhotic patients, because, with time, the differences may be cumulative. However, whether this hypermetabolism can lead to a real weight loss remains to be evaluated in a longitudinal study.
Raynaud's phenomenon is an intermittent vasospasm of the arterioles of the distal limbs which occurs mostly following exposure to cold or emotional stimuli. Helicobacter pylori infection, the most relevant cause of gastritis, has been associated with some vascular diseases. The aim of this study was to assess the prevalence of H. pylori infection and effects of eradication on Raynaud attacks. Twenty-five patients affected by primary Raynaud's phenomenon were evaluated. H. pylori infection was assessed by the 13C urea breath test and 20 subjects were found to be infected by the bacterium. Triple therapy consisting of amoxicillin, clarithromycin, and lansoprazole was given to the patients for 7 days at the time of diagnosis. Duration and frequency of clinical attacks of Raynaud's phenomenon per week were assessed for 12 weeks after eradication. In 80 percent of the patients Raynaud's was eradicated after therapy. Clinical attacks of Raynaud's phenomenon completely disappeared in 18% of the eradicated patients. Duration and frequency of attacks were significantly reduced in 68% of the remaining patients. The preliminary findings from this study show that H. pylori eradication significantly ameliorates primary Raynaud's disease.
H. pylori infection has recently been associated with various vascular disorders. The aim of this study was to investigate its role in primary headache, a pathology strictly associated with vascular alterations. A total of 200 subjects affected by primary headache were evaluated. H. pylori infection was diagnosed by the 13C urea breath test. Headache was classified in tension-type headache, cluster headache, and migraine with or without aura. Prevalence of H. pylori infection and gastrointestinal (GI) symptoms were evaluated. H. pylori infection was found in 40% of the patients; prevalence of migraine without aura was found to be significantly greater in infected patients. The positive group showed no significant differences in the prevalence of the GI symptoms evaluated. In 30 infected patients, it was assessed whether the eradication of the bacterium was able to reduce frequency, intensity, and duration of clinical attacks of headache. After eradication, clinical attacks of headache completely disappeared in 17% of patients. Moreover, intensity, duration, and frequency of headache attacks were reduced in 69% of the remaining subjects. In conclusion, H. pylori infection is common in primary headache; bacterium eradication appears to be related to a significant reduction in clinical attacks of the disease.
BACKGROUND/AIMS: This study aimed to assess the main features of hepatocellular carcinoma at the time of diagnosis in Italy, particularly in relation to the presence or absence of underlying cirrhosis, hepatitis virus marker patterns, age of the subjects and alpha-foetoprotein values. METHODS: A total of 1148 patients with hepatocellular carcinoma seen at 14 Italian hospitals in the 1-year period from May 1996 to May 1997 were the subjects of this prevalence study. Both newly diagnosed cases (incident cases) and cases diagnosed before May 1996 but still attending the hospitals during the study period (prevalent cases) were included. RESULTS: We found that 71.1% of cases were positive for hepatitis C virus antibodies but negative for HBsAg; in contrast, 11.5% were negative for anti-HCV but positive for HBsAg; 5.3% were positive for both markers; and 12.1% were negative for both viruses. The mean age of detection was over 60 years, with a younger mean age in HBsAg-positive compared to anti-HCV-positive patients (59.3 years vs. 65.6 years, p<0.01). The male-to-female ratio among HBsAg-positive patients was 10.4:1, in contrast to 2.8:1 among anti-HCV-positive patients (p<0.01). The majority of cases (93.1%) had underlying cirrhosis. Cirrhotic patients were more likely to be anti-HCV positive than non-cirrhotic cases (73.2% vs 43.9%; p<0.01); conversely, absence of hepatitis virus markers was more frequently observed in the non-cirrhotic than in the cirrhotic population (40.9% vs. 10.0%; p<0.01). Overall, the alpha-foetoprotein level was altered (>20 ng/ml) in 57.9% of patients; only 18% of cases presented diagnostic (>400 ng/ml) values. Anti-HCV positivity (O.R. 2.0; CI 95%=1.3-3.1) but not HBsAg positivity (O.R. 1.0; CI 95%=0.6-1.8) was shown to be an independent predictor of the likelihood of altered alpha-foetoprotein values by multivariate analysis. CONCLUSIONS: These findings point to differences in the characteristics of the populations infected by hepatitis B and hepatitis C. Factors other than the hepatitis viruses are important in non-cirrhotic patients. A change in the relative prevalence of hepatitis virus markers among hepatocellular carcinoma cases was demonstrated, reflecting a significant change in the rate of HBV endemicity in the Italian population. Finally, the increased trend in the mortality rate from liver cancer in Italy from 4.8 per 100,000 in 1969 to 10.9 in 1994 may reflect the large cohort of subjects infected with HCV via the iatrogenic route during 1950s and 1960s when glass syringes were commonly used for medical treatment.
Dodecanedioic acid (C12) is an even-numbered dicarboxylic acid (DA). Dicarboxylic acids are water-soluble substances with a metabolic pathway intermediate to those of lipids and carbohydrates. Previous studies showed that contrary to other DAs, very low amounts of C12 are lost with urine. The effects of 46.6 mmol of C12 intravenous infusion for 195 min on blood glucose levels were investigated in five patients with non-insulin-dependent diabetes mellitus (NIDDM), with a good metabolic compensation, and in five healthy volunteers matched for gender, age, and body mass index. Blood samples were taken every 15 min for a period of 360 min to measure glucose, insulin, C-peptide, ketone bodies, and free fatty acid (FFA) levels, and 24-h urine samples were collected to measure C12 and urea excretion. Plasma and urinary C12 concentrations were determined by high-pressure liquid chromatography (HPLC). Indirect calorimetry was continuously performed both basally and during the study period. The average 24-h urinary excretion of C12 was 6.5% versus 6.7% of the administered dose, respectively, in NIDDM patients and in healthy controls. The area under the curve (AUC) values of plasma C12 were 279.9 +/- 42.7 mumol in NIDDM patients and 219.7 +/- 14.0 mumol in controls (P = ns). Plasma glucose levels significantly decreased in NIDDM patients during C12 infusion (from 7.8 +/- 0.6 to 5.4 +/- 0.8 mM at the end of the study period, P < 0.05). Lactate plasma concentration decreased in NIDDM patients from 3.5 +/- 0.2 to 1.5 +/- 0.1 mM (P < 0.001), whereas blood pyruvate increased at the end of the experimental session from 26.0 +/- 11.6 to 99.5 +/- 14.9 microM (P < 0.01). Free fatty acids decreased in diabetic patients from the beginning until the end of C12 infusion, although this difference did not reach statistical significance. No significant increase was found between basal and final values in VO2 consumption and in the values of nonprotein respiratory quotient in both groups of subjects examined. The experimental data indicate that C12 infusion decreases plasma glucose levels in NIDDM patients to normal range without influencing plasma insulin levels. The balance between pyruvate and lactate was affected by C12 infusion only in diabetics patients. C12 might represent a fuel substrate immediately available for tissue energy requirements, especially in conditions such as diabetes mellitus in which glucose metabolism is impaired.
The relationship between chronic moderate beer consumption and oxidative stress was studied in rats. Animals were fed three different isocaloric diets for six weeks: a beer-containing diet (30% w/w), an ethanol-supplemented diet (1.1 g/100 g, the same as in the beer diet) and an alcohol-free basal diet. At the end of the feeding period, rats were analyzed for plasma and liver oxidative status. Some livers were isolated and exposed to ischemia-reperfusion to assess the additional oxidative stress determined by reperfusion. No significant differences in plasma antioxidant status were found among the three dietary groups. Lipoproteins from the beer group, however, showed a greater propensity to resist lipid peroxidation. Ischemia caused a decrease in liver energy and antioxidant status in all groups. Nevertheless, ATP was lower in the livers of rats exposed to the ethanol diet. During reperfusion, lipoperoxidation increased significantly in all groups. However, livers obtained from ethanol-treated rats showed the higher formation of lipoperoxides. In conclusion, a moderate consumption of beer in a well-balanced diet did not appear to cause oxidative stress in rats; moreover, probably through its minor components, beer could attenuate the oxidative action of ethanol by itself.
Raynaud's phenomenon is defined by an intermittent vasospasm of the arterioles of the distal limbs. Helicobacter pylori infection has been recently associated with Raynaud's phenomenon. The aim of this study was to assess the effects of H. pylori eradication on Raynaud's attacks. Forty-six patients affected by primary Raynaud's phenomenon were evaluated. H. pylori infection was assessed by [13C]urea breath test. Eradication therapy was given to infected patients for seven days. Discomfort and the duration and frequency of attacks of Raynaud's phenomenon per week were assessed. Thirty-six subjects were infected with H. pylori; the bacterium was eradicated in 83% of these after therapy. Attacks of Raynaud's phenomenon completely disappeared in 17% of the patients with H. pylori eradication. Discomfort and the duration and frequency of attacks of Raynaud's phenomenon were significantly reduced in 72% of the remaining patients. Conversely, attacks of Raynaud's disease did not change significantly during the 12-week follow-up period either in the H. pylori-negative patients or in the infected subjects in whom the bacterium was not eradicated by therapy. The study shows that H. pylori eradication causes a significant decrease in clinical attacks of Raynaud's disease. The reduction of vasoactive substances determined by the eradication of the bacterium may be the pathogenetic mechanism underlying the phenomenon.
Helicobacter pylori, the most important cause of gastritis and peptic ulcer, recently has been associated with several extradigestive diseases. The aim of this study was to assess the prevalence of Helicobacter pylori infection and the effects of bacterium eradication in 42 consecutive patients affected by idiopathic chronic urticaria. Helicobacter pylori was assessed by [13C]urea breath test. Amoxicillin, clarithromycin, and lansoprazole were given to infected patients for seven days. Urticaria and gastrointestinal symptoms were assessed on enrollment and after eradication. Fifty-five percent of patients proved to be infected by Helicobacter pylori. Prevalence of gastrointestinal symptoms did not differ between infected and uninfected patients. Eighty-eight percent of infected patients in whom the bacterium was eradicated after therapy showed a total or partial remission of urticaria symptoms. Conversely, symptoms remained unchanged in all uninfected patients. In conclusion, Helicobacter pylori affects a high percentage of patients with idiopathic chronic urticaria; however, typical gastrointestinal symptoms do not identify infection status. Bacterium eradication is associated with a remission of urticaria symptoms, suggesting a possible role of Helicobacter pylori in the pathogenesis of this skin disorder.
Heat shock proteins are intracellular proteins associated with a generalized response of cells to stress. The purpose of this study was to assess RNA levels of heat shock protein 70 and 90 in fed or fasted rat livers during ischemia-reperfusion. Northern blot analysis of heat shock proteins was performed. Adenosine triphosphate and glutathione were assessed. In baseline conditions, livers of fasted rats showed a twofold increase in mRNA for both heat shock proteins and 38% and 43% reductions in adenosine triphosphate and glutathione, respectively, when compared with organs from fed rats. After ischemia, livers of fasted rats presented a twofold decrease in heat shock protein mRNA, while no changes were observed in livers of fed rats; reduced glutathione and adenosine triphosphate decreased 55% and 50% in fasted livers and 25% and 20% in fed organs, respectively. After 120 min of reperfusion, heat shock protein mRNA rose threefold in fasted livers, while a slight decrease was observed in the fed group; reduced glutathione and adenosine triphosphate returned to 65% and 70% of baseline values in fasted livers and 85% and 90% in fed organs, respectively. In conclusion, the nutritional status affects heat shock protein expression determined by reperfusion. The reduced antioxidant status leading to increased oxidative stress could be the mechanism underlying the phenomenon.
BACKGROUND: Obesity is characterised by growth hormone (GH) abnormalities, including a blunted response to stimulation and a 'paradoxical' increase after meals. The blunted GH release is reversed by a surgical intestinal bypass procedure. However, this does not mean that normal GH dynamics have been restored. The present study assessed whether post-surgical weight reduction in obese patients normalised the modulation of GH release produced by metabolic fuels. SUBJECTS: Ten obese female subjects, aged 23-54 y, were studied before and after biliopancreatic diversion (BPD). All patients, after surgery, had experienced a significant reduction in body weight (mean body mass index (BMI) 25.78 +/- 1.01 kg/m2 vs 44.68 +/- 1.73 kg/m2). Two groups were also studied as controls: Ten normal body weight female subjects and ten patients suffering from anorexia nervosa (AN, mean BMI 17.46 +/- 1.12 kg/m2). MEASUREMENTS: We have studied the GH response to a GH releasing hormone (GHRH) bolus (1 microg/kg i.v., at 13.00 h) before and after a standard meal. RESULTS: In post-BPD subjects, the GH response to GHRH in the fasting state, was clearly augmented in comparison with the pre-BPD values (peak values 18.06 +/- 4.56 vs 3.24 +/- 0.68 microg/L). In post-BPD subjects the postprandial GH response was further augmented in comparison with the fasting test (peak 30.12 +/- 4.99 microg/L, P < 0.05). This pattern was similar to that observed in anorexic patients. CONCLUSION: The surgical procedure restores a normal GH response to GHRH in the fasting state, but the 'paradoxical' GH response after meals remains present, suggesting a persistent GH derangement in such patients, which is not related to body weight per se. The surgical procedure makes obese patients similar to anorexics, in the relationships between metabolic fuels and GH secretion. The persistence of the GH postprandial response to GHRH in post-BPD subjects suggests a role for metabolic fuels in the regulation of somatostatin (SRIF) secretion.
BACKGROUND: One-week ranitidine bismuth citrate (RBC)-based triple regimens may be effective for the eradication of Helicobacter pylori. We evaluated the efficacy of two short-term RBC-based eradicating therapies including RBC plus medium-dose clarithromycin and either tinidazole or amoxycillin. METHODS: Seventy consecutive patients, who underwent gastroscopy for dyspeptic symptoms and were found to be H. pylori-positive, were randomly subdivided into two groups receiving either RBC 400 mg b.d. plus clarithromycin 250 mg t.d.s. and tinidazole 500 mg b.d. (group RBCCT) or RBC 400 mg b.d. plus clarithromycin 250 mg t.d.s. plus amoxycillin 1 g b.d. (group RBCCA). H. pylori status was evaluated by means of histology and rapid urease test at entry, and by 13C-urea breath test alone 8 weeks after treatment. RESULTS: Sixty-nine out of 70 enrolled patients completed the study: 35/35 in group RBCCT and 34/35 in group RBCCA. One patient in group RBCCA was lost to follow-up. In group RBCCT, at the end of treatment, 32 of 35 patients were H. pylori-negative (per protocol analysis 91%, intention-to-treat analysis 91%; 95% CI: 77-98%). In group RBCCA, 31 of 34 patients returned H. pylori-negative (per protocol 91%; 95% CI: 76-98%, intention-to-treat 89%; 95% CI: 73-97%). Slight side-effects occurred in 3/35 patients (9%) in group RBCCT and in 3/34 (9%) in group RBCCA. CONCLUSIONS: One-week regimens consisting of RBC plus clarithromycin and either tinidazole or amoxycillin, combine high eradication rates with modest side-effects. No substantial difference was found between the two treatment regimens tested in this trial.
OBJECTIVES: To evaluate the anthropometric and metabolic characteristics of patients with Crohn's disease (CD) and ulcerative colitis (UC), comparing both groups with healthy volunteers. DESIGN: A cross-sectional study. SETTING: The Department of Internal Medicine, Catholic University Hospital, Rome, Italy. SUBJECTS: Thirty-four patients with biopsy-proven inflammatory bowel disease (18 CD; 16 UC) in clinical remission (SCDAI < 3 and Powell-Tuck index < 4) not receiving steroid therapy. INTERVENTIONS: All patients had a clinical examination. MAIN OUTCOME MEASURES: Blood indicators of inflammation and nutritional status. Body composition was assessed by both anthropometry and bioimpedance and metabolic variables were measured by indirect calorimetry over a 60-90 min period. RESULTS: CD had a lower body weight than both controls (58.1 kg, range 41.5-71.0 vs. 66.4 kg, range 57.0-76.0; P < 0.001) and UC) 58.1 kg, range 41.5-71.0 vs. 69.6 kg, range 50.5-94.0; (P < 0.001). Fat-free mass (FFM) did not differ between the groups, whilst fat mass was significantly lower in CD than in UC (P < 0.05) and controls (P < 0.001). Normalizing the basal metabolic rate by FFM, a higher value was found in CD compared with UC (143 kJ kg-1) d-(-1), range 97.5-179 vs. 133 kJ kg-1 d-1, range 123-148; P < 0.05) and control subject 143 kj kg-1 d-1, range 97.5-179 vs. 134 kj kg-1 d-1, range 122-162; P < 0.05). The nonprotein respiratory quotient was significantly lower in CD compared to UC 0.80, range 0.73-0.84 vs. 0.84, range 0.79-0.91; P < 0.01) and controls (0.80, range 0.73-0.84 vs. 0.83, range 0.81-0.87; P < 0.001), with a consequently higher lipid oxidation rate in CD. CONCLUSIONS: CD subjects showed a decreased fat mass and enhanced utilization of lipids compared with UC and controls. These data could be explained by the larger intestinal involvement and considered as a contribution to lipid tissue wasting in CD.
OBJECTIVES: To evaluate the influence of chronic alcohol abuse on body composition and energy metabolism in patients affected by chronic alcoholism (group A) compared with a group of healthy social drinkers (group B). SETTING: A university hospital clinic in Italy. SUBJECTS: A total of 32 alcoholics without clinical or laboratory signs of liver cirrhosis and malabsorption. MEASUREMENTS: Body composition was assessed by anthropometric measurements. Resting energy expenditure (REE) and substrate oxidation rate was measured by indirect calorimetry. Daily caloric intake was computed on the basis of a food diary compiled over 7 days. RESULTS: Alcoholics showed a significantly lower body weight (P < 0.05) and a significant lower fat mass (P < 0.05) compared with controls. A higher waist-to-hip ratio was found in group A than in group B, both as a whole group (P < 0.01) or separated by gender (females, P < 0.01) and males, P < 0.001), indicating a prevalence of fat distribution in the abdominal region in alcoholics. REE was significantly higher in group A than in group B (P < 0.05). The non-protein respiratory quotient was significantly lower in group A than in group B (P < 0.001) with a consequent higher utilization of lipids (P < 0.01) and a lower carbohydrate oxidation (P < 0.05) in group A. The energy intake provided only by food ingestion was found to be significantly higher in group B (P < 0.01), whilst the total caloric intake, computed as food intake plus alcohol intake, was higher in group A (P < 0.01). CONCLUSIONS: Alcoholics, as compared with social drinkers, showed a lower body weight due essentially to a fat mass reduction, a higher REE value normalized by fat-free mass, and a preferential utilization of lipids as energy substrate. These findings might suggest that chronic ethanol abuse is able to determine an impairment of nutritional status due, at least in part, to an alteration of the substrate oxidation.
BACKGROUND: Mucosa-associated lymphoid tissue (MALT) develops in gastric mucosa in response to chronic antigenic stimulation, such as Helicobacter pylori infection. However, reactive lymphoid follicles have been found also in the stomach of H. pylori-negative coeliac patients, suggesting that other environmental factors may be involved in MALT genesis. The aim of our study was to evaluate the effects of gluten withdrawal in H. pylori-negative coeliac patients with gastric MALT. METHODS: We studied 23 H. pylori-negative untreated coeliac patients with gastric MALT. All patients underwent determination of antigliadin (AGA) and antiendomysium antibodies (EMA) and upper endoscopy with multiple biopsies in duodenum, gastric corpus, and antrum. Lymphoid follicles and H. pylori status were assessed by histopathologic and enzymatic analysis. All patients were started on a gluten-free diet and were reevaluated after 12 months. To consider their adherence to the gluten-free diet we relied on direct patient questioning. Thirteen patients who had strictly adhered to the gluten-free diet constituted our study group. Ten patients who had not strictly adhered to gluten withdrawal from their diet constituted the control group. RESULTS: Regression of MALT was obtained in 9 of 13 (69%) patients who strictly followed the gluten-free diet; in the control group MALT disappeared in 2 of 10 (20%) patients (P=0.0361). DISCUSSION: Disappearance of reactive lymphoid follicles in the gastric mucosa of H. pylori-negative coeliac patients after gluten withdrawal suggests that antigens related to alimentary gluten may constitute persistent stimuli for development of gastric MALT in coeliac patients.
BACKGROUND: Whipple's disease, like other malabsorption syndromes, ought to predispose to osteopenia. We therefore evaluated bone mass and mineral metabolism in a cohort of patients with this condition. METHODS: Twelve male patients with Whipple's disease and 36 male age-matched healthy subjects took part in the study. None of the patients complained of diarrhea at the time of the study. Bone mineral density at the lumbar and femoral level and serum levels of indices of bone and mineral metabolism and of gonadal function were measured. RESULTS: Bone mineral density at the total femur and femoral neck were significantly lower in patients with Whipple's disease than in healthy volunteers, whereas no significant difference was found at the lumbar level. In patients with Whipple's disease serum levels of type-I collagen teleopeptide (ICTP) and sex-hormone-binding globulin were significantly higher, whereas serum levels of testosterone and luteinizing hormone were significantly lower than in healthy volunteers. Moreover, testosterone correlated significantly (P < 0.05) with lumbar bone mineral density (r(s) = 0.64) and serum ICTP levels (r(s) = -0.63). CONCLUSIONS: In patients with previously treated Whipple's disease and without any current symptoms of malabsorption, bone loss is generally moderate and linked to the presence of hypogonadism.
BACKGROUND: The reoxygenation phase after a period of anoxia leads to oxyradical formation, responsible for damage to cell membranes. Ageing is associated with functional and structural changes in liver cells, which modify their sensitivity to reoxygenation injury. The aim of this study was to determine the effects of ageing on the sensitivity of hepatocytes to anoxia/reoxygenation. METHODS: Oxyradical formation and cell injury were evaluated in hepatocytes isolated from rats of different ages exposed to 2 h of anoxia and 1 h of reoxygenation. Anion superoxide was measured by lucigenin-enhanced chemiluminescence, hydrogen peroxide by luminol-enhanced chemiluminescence, and cell damage by lactate dehydrogenase (LDH) release. RESULTS: During anoxia, oxyradical production dropped to background levels in both groups. LDH release was significantly greater in ageing hepatocytes. During reoxygenation, a massive generation of anion superoxide and hydrogen peroxide, followed by a sharp increase in LDH release, was observed in both groups. However, both oxyradicals and cell injury were significantly greater in liver cells obtained from ageing rats. CONCLUSIONS: The data confirm that hepatocytes produce high levels of free radicals during post-ischemic reoxygenation and suggest that ageing cells are more sensitive to reperfusion injury.