Fernando de Ritis

An evaluation of urinaryd-glucaric acid excretion during acute hepatitis in man

The excretion of urinaryd-glucaric acid (d-GA), one of the final metabolites of glucuronic acid was determined in 49 patients with acute hepatitis. A 3.7-fold increase ofd-GA was found at an early stage of the disease (37.13 μmol/24hr±3.08se vs 9.91 μmol/24hr±1.18se in normal controls), when serum transaminases and bilirubin were very high (SGOT 589 I.U.±41se; SGPT 954 I.U.±61se; serum bilirubin 8.41 mg/100 ml±0.76se). A lower but significantly elevatedd-GA excretion was also found in the recovery phase of hepatitis at a time when both serum transaminases and bilirubin were considerably reduced (SGOT 89 I.U.±14se; SGPT 185 I.U.±30se; serum bilirubin 1.05 mg/100 ml±0.20se). Urinary glucuronides and free glucuronic acid, measured as total glucuronic acid, were also significantly increased in early hepatitis (1164 mg/24hr±54se vs 782 mg/24hr±84se in normal subjects), but no correlation was found withd-GA excretion. A short treatment with phenobarbital which led to a 3-fold increase ofd-glucaric acid in 12 normal subjects did not cause any further change in the patients with early acute hepatitis. While the mechanism of the urinaryd-GA increase in hepatitis still remains underfined, the findings of this study support the conclusion that its increase may not reflect an induction of liver microsomal enzymes.

Serum enzymes (transaminases, phosphoglucomutase, fumarase) in viral hepatitis during prednisone (δ1-cortisone) therapy

Abstract The pattern of some enzyme activities (transaminases, phosphoglucomutase, fumarase) has been investigated in cases of virus hepatitis during treatment with prednisone (δ 1 -cortisone). This steroid therapy seems to suppress readily some serum enzyme activities and to diminish others promptly. The theoretical and pathogenetic background of this observation is briefly discussed.

Nucleoside Phosphates in Liver of Mice During Experimental MHV-3 Virus Hepatitis.

Summary The concentration of nucleoside phosphates was determined in the liver of mice at various intervals after experimental infection with MHV-3 virus. During the first phase of active viral multiplication, occurring between 12 and 24 hours after inoculation of virus, there was no change in concentration of the nucleoside phosphates. A significant decrease only in nucleoside triphos-phates was first found at 36 hours after inoculation when hepatic necrosis is only initial. This decrease became more marked at 48 and 72 hours at which time there also appeared a statistically significant decrease in nucleoside di- and mono-phosphates.

Attività esochinasi del cervello e del miocardio nella infezione sperimentale da virus dell'encefalomiocardite (EMC)

The hexokinase activity in brain and myocard of mice infected with EMC virus by the intracerebral route increases gradually from the 14th hour p. i. to a statistically significant value at the 18th hour p. i. and to a maximum (+ 30.39% for brain, 50.5% for myocard) at the 24th hour p. i.; at the 30th hour p. i., when first death of animals occurs, the increase is no longer statistically significant.The hexokinase activity in brain and myocard of mice infected with EMC virus by the intracerebral route increases gradually from the 14th hour p. i. to a statistically significant value at the 18th hour p. i. and to a maximum (+ 30.39% for brain, 50.5% for myocard) at the 24th hour p. i.; at the 30th hour p. i., when first death of animals occurs, the increase is no longer statistically significant. The results are briefly discussed in relation to the importance of the phosphorylative and glycolytic activities of the host cell in response to the viral multiplication and its pathogenic effect.

Studio biochimico dell'infezione sperimentale da virus dell'encefalomiocardite. Comportamento di alcune attività enzimatiche nel cervello, nel fegato e nel miocardio (adenilpirofosfatasi, succinodeidrogenasi, aspartico-chetoglutarico transaminasi, rodanese)

The determination of enzymatic activities (adenylpyrophosphatase, transaminase, succinodehydrogenase, rhodanese) in the brain, liver and myocard of mice infected with EMC virus both by the intraperitoneal and intracerebral route, yielded the following results: 1. Adenylpyrophosphatase: Statistically significant increase in all tested tissues of animals infected by both routes. 2. Aspartic-ketoglutaric transaminase: Statistically significant decrease in the liver and brain and myocard of mice infected by intraperitoneal route. Statistically significant decrease in the only liver and myocard of mice infected by intracerebral route. 3. Succinodehydrogenase: Statistically significant increase in the brain of mice infected by both routes. In the liver a significant variation has not been observed. 4. Rhodanese: Statistically significant decrease in the brain and liver only after intracerebral infection. In the intraperitoneally infected animals such a significant variation has not been observed. Adenylpyrophosphatase: Statistically significant increase in all tested tissues of animals infected by both routes. Aspartic-ketoglutaric transaminase: Statistically significant decrease in the liver and brain and myocard of mice infected by intraperitoneal route. Statistically significant decrease in the only liver and myocard of mice infected by intracerebral route. Succinodehydrogenase: Statistically significant increase in the brain of mice infected by both routes. In the liver a significant variation has not been observed. Rhodanese: Statistically significant decrease in the brain and liver only after intracerebral infection. In the intraperitoneally infected animals such a significant variation has not been observed. The results are briefly discussed from the point of view of metabolic interpretation of the pathogenetic mechanism of viral infection.

Attività della imide dell'acido maleico (n-etyl-maleimide) sulla moltiplicazione virale

1. The action of an imide of maleic acid (N-etyl-maleimide) on the multiplication of influenza virus in allantoic cavity of chick embryo as deduced by the hemoagglutinating titer has been investigated. 2. The eggs were injected with 1 LD32 (0,003 M) maleimide into the yolk sac 48-24-12-0 hours before allantoic infection with 3 ID50 of the PR 8 strain of influenza virus. Allantoic fluids were harvested after 6, 12, 24, 48 hours of incubation at 37° C and individually titrated for hemoagglutinating titer accordingSalks technique. 3. The growth of virus which began at the 6th hour in the controls was completely inhibited in the chick embryos previously injected with maleimide, irrespective of the length of the period between the injection of the maleimide and the virus infection. The inhibition of virus multiplication persisted until the 24th hour of incubation; after this period virus growth began. Between the 24th and the 48th hour the hemoagglutinating titers of the fluids of the normal and of the maleimido-treated chick embryos showed no significant difference. 4. The results of the experiment were analysed by the methods of variance analysis and of means comparison (t ofStudent). Both statistical methods fully confirm the high significance of the results observed. 5. The virus-growth inhibition by maleimide has been discussed in relation to the capacity of this compound to inhibit sulphydryl groups and to the sulphydryl requirement of protein synthesis. The action of an imide of maleic acid (N-etyl-maleimide) on the multiplication of influenza virus in allantoic cavity of chick embryo as deduced by the hemoagglutinating titer has been investigated. The eggs were injected with 1 LD32 (0,003 M) maleimide into the yolk sac 48-24-12-0 hours before allantoic infection with 3 ID50 of the PR 8 strain of influenza virus. Allantoic fluids were harvested after 6, 12, 24, 48 hours of incubation at 37° C and individually titrated for hemoagglutinating titer accordingSalks technique. The growth of virus which began at the 6th hour in the controls was completely inhibited in the chick embryos previously injected with maleimide, irrespective of the length of the period between the injection of the maleimide and the virus infection. The inhibition of virus multiplication persisted until the 24th hour of incubation; after this period virus growth began. Between the 24th and the 48th hour the hemoagglutinating titers of the fluids of the normal and of the maleimido-treated chick embryos showed no significant difference. The results of the experiment were analysed by the methods of variance analysis and of means comparison (t ofStudent). Both statistical methods fully confirm the high significance of the results observed. The virus-growth inhibition by maleimide has been discussed in relation to the capacity of this compound to inhibit sulphydryl groups and to the sulphydryl requirement of protein synthesis.