(+ )-Cyanidanol-3 in Acute Viral Hepatitis

Nola, F Di

doi:10.1016/s0140-6736(80)92457-5

Cited by 8 publications

(3 citation statements)

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“…The flavonoid cianidanol (( + )-cianidanol-3) has been used for the treatment of hepatitis in several countries for several years (Blum et aJ. 1977: Di Nola, 1980: Schomerus et nl, 1984: Piazza et nl, 1983. Recently the drug was associated with episodes of life-threatening intravascular haemolysis in some patients, the pathogenesis of which is as yet unknown.…”

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“…Recently the drug was associated with episodes of life-threatening intravascular haemolysis in some patients, the pathogenesis of which is as yet unknown. In only two of the reported cases drug-dependent antibodies (ddab) against RBC were recognized (Neftel et aJ, 1980;Heim et aJ, 1982: Pausch & Gobel, 1983. We had the opportunity to study six patients with this syndrome.…”

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Cianidanol and its metabolites bind tightly to red cells and are responsible for the production of auto‐ and/or drug‐dependent antibodies against these cells

Salama

Mueller‐Eckhardt

1987

Br J Haematol

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Cianidanol ((+)-2-(3,4-dihydroxyphenyl)-3, 5, 7-chromantriol) is a flavonoid which has been associated with severe immune haemolysis by as yet unclear mechanisms. We report six patients who developed haemolysis while receiving the drug. The disorder was episodic in all patients and resolved after discontinuing the drug. The causative antibodies could be demonstrated in all six cases, even when the haemolytic episode was more than 1 year prior to this study. One patient had developed drug-independent IgG autoantibodies, another simultaneously developed autoantibodies and drug-dependent antibodies (ddab) of the IgG class, while the remaining four patients had only ddab of the IgM and/or the IgG classes. All ddab were reactive with red blood cells (RBC) in the presence of the drug and/or its metabolites (ex vivo antigens), and, quite unexpectedly, also with RBC coated with the drug (metabolites) in vitro or in vivo. This reactivity did not change either by preincubating the antibodies with the drug or by adding large amounts of the drug to the mixture of drug-coated cells plus antibody. It seems that the stable association of cianidanol with RBC generates antigenic sites against which a heterogeneous immune response is elicited giving rise to long-lasting drug-dependent antibodies as well as autoantibodies.

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Cianidanol and its metabolites bind tightly to red cells and are responsible for the production of auto‐ and/or drug‐dependent antibodies against these cells

Salama

Mueller‐Eckhardt

1987

Br J Haematol

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“…α-Tocopherol is the most biologically potent antioxidant of the four tocopherols that together constitute vitamin E (10). The flavonoid (+)-cyanidanol-3 (CND), also named (+)-catechin, is a naturally occurring flavonoid that has been shown to exert a number of liver-protecting actions: improvement of hepatic parenchimal regeneration, stabilization of the biomembrane structure by scavenging free radicals, and stimulation of certain types of immune function (11). CND has antioxidant properties and has been investigated in a number of LPO studies with liver, kidney and brain as target organs (12,13).…”

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Protection against cephalosporin-induced lipid peroxidation and nephrotoxicity by (+)-cyanidanol-3 and vitamin E

Cojocel

Tolle

El-Hajj

et al. 2007

Braz J Med Biol Res

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The ability of the clinically used cephalosporins: cephalothin, cefotaxime and cefotiam to induce lipid peroxidation (LPO) and renal damage was compared to that of nephrotoxic cephaloridine under in vivo conditions. Glutathione was measured in rat liver or in renal cortex as non-protein sulfhydryls. LPO was measured in plasma, renal cortex and liver by the generation of malondialdehyde or as the increase in renal cortical concentration of conjugated dienes. Impairment of renal function was measured as the decrease in renal cortical accumulation of the organic anion p-aminohippurate (PAH). Administration of cephalosporins to rats as a single dose (2000 mg/kg, ip) induced a significant glutathione-depletion in the renal cortex with cephaloridine, and in the liver with cephaloridine, cephalothin and cefotiam. Treatment of rats with cephaloridine, cephalothin and cefotiam (200, 500, or 1000 mg kg -1 day -1 , ip) for 5 days resulted in a dose-dependent increase of LPO in the renal cortex. While cephaloridine induced the highest concentration of conjugated diene, cefotaxime had no effect. Measurements of PAH accumulation in renal cortical slices from cephalosporin-treated rats showed a dose-dependent decrease in the renal cortical accumulation of PAH. Pretreatment with the antioxidants vitamin E or cyanidanol (400 mg kg -1 day -1 , ip) 1 h before treatment with cephaloridine, cephalothin or cefotiam (1000 mg kg -1 day -1 , ip) for 3 days inhibited cephalosporin-induced LPO and significantly reduced the impairment of renal cortical accumulation of PAH. The potential of different cephalosporins for inducing LPO and reducing PAH accumulation was ranked as follows: cephaloridine > cephalothin > cefotiam > cefotaxime.

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