Methyl hesperidin

Carcinogenicity study of methyl hesperidin in B6C3F1 mice.[Pubmed:2272558]

Food Chem Toxicol. 1990 Sep;28(9):613-8.

A long-term carcinogenicity study of Methyl hesperidin, a compound of the vitamin P group, was carried out in B6C3F1 mice receiving dietary concentrations of 0, 1.25 or 5%. Administration was continued for 96 wk and then the mice were maintained on basal diet for an additional 8 wk. Growth retardation during the experiment with final changes in organ weights were observed in females given the 1.25% dose of Methyl hesperidin and in both sexes receiving the 5.0% treatment. However, no biologically significant effects were evident with respect to mortality or clinical signs. Furthermore, treatment with Methyl hesperidin did not result in any changes in haematology, clinical chemistry and urinalysis data. On histological examination, no significant alteration of non-neoplastic and neoplastic lesion incidence was observed in treated mice. The results thus demonstrated that Methyl hesperidin lacked any carcinogenicity for B6C3F1 mice in the 96-wk feeding regimen used in this study.

Influence of some bioflavonoids on the transport of nitrendipine.[Pubmed:19326773]

Drug Metabol Drug Interact. 2008;23(3-4):299-310.

Flavonoids form a large class of phenolic substances widely distributed in nature and exhibit several biological effects. P-glycoprotein is part of a large family of efflux transporters found in the gut, gonads and other organs. Male albino rats were used for this study. The whole small intestine was flushed with 50 ml of ice-cold saline after sacrificing the animal with an overdose of pentobarbital. The small intestine was isolated and divided into duodenum, jejunum and ileum. Each segment was everted, a 5-cm long sac was prepared, 1 ml of nitrendipine solution was introduced into the everted sac (serosal side), and both ends of the sac were ligated tightly. The sac containing nitrendipine solution was immersed in 30 ml of Dulbecco's phosphate buffer solution (D-PBS) containing 25 mM glucose and the same concentration of different bioflavonoids, viz., diosmin, quercetin, chrysin, Methyl hesperidin and gossypin, was introduced into the mucosal side. Transport of nitrendipine from serosal to mucosal surfaces across the intestine was determined by collecting samples from the mucosal medium periodically at different intervals: 0, 10, 20, 30, 60, 90 and 120 minutes. The samples were analyzed by HPLC. Diosmin and quercetin decreased the transport rate of nitrendipine to nearly the same extent in all regions. Chrysin and gossypin decreased the transport rate of nitrendipine to a greater extent in the ileum than in the duodenum and jejunum. Methyl hesperidin caused inhibition of nitrendipine transport in the ileum and jejunum, but not in the duodenum. All bioflavonoids, i.e., quercetin, diosmin, Methyl hesperidin, gossypin and chrysin, decreased the transport of nitrendipine, a P-gp substrate in the rat intestine. The highest expression of P-gp was found in the ileum followed by the jejunum and duodenum.

Subchronic toxicity study of methyl hesperidin in mice.[Pubmed:8356566]

Toxicol Lett. 1993 Jul;69(1):37-44.

A subchronic toxicity study of Methyl hesperidin was performed using B6C3F1 mice. The flavonoid was administered to groups of ten males and ten females in dietary levels of 0, 0.3, 0.6, 1.25, 2.5 and 5.0% for 13 weeks. No significant treatment-related differences were found in data for body weights, food and water consumption, hematology, clinical chemistry and organ weights. Furthermore, no effects of treatment were observed on gross and histopathological examination of the major organs. The present experiment thus demonstrated that Methyl hesperidin exerts no obvious toxic effects in mice of either sex when administered at a level as high as 5.0% in the diet.