In vivo antimutagenic and antiatherogenic effects of the (1 → 3)(1 → 6)-ß-d- glucan botryosphaeran.

The antimutagenic effect of botryosphaeran, an exocellular (1 → 3)(1 → 6)-ß-d-glucan, from the ascomyceteous and plant-borne endophytic fungus, Botryosphaeria rhodina MAMB-05, was evaluated in young (6-8 weeks) and elderly (18 months) Swiss albino mice of both genders. The hypolipidemic, hypoglycemic and antiatherogenic potential was also evaluated in 18-month old male LDL receptor knockout (LDLr-/-) mice. Administration of botryosphaeran by gavage (doses: 7.5, 15, 30 mg/kg b.w./day) in a 30-day pretreatment protocol (young mice), or 15-day protocol (older mice), did not cause genotoxicity as assessed by the micronucleus test in peripheral blood (PB) and bone marrow cells (BMCs). Furthermore, there was no cytotoxic effect of this ß-d-glucan in the treatments. A lower frequency of micronuclei was observed in BMCs from young and old mice that received botryosphaeran, indicating its antimutagenic effect. Botryosphaeran (30 mg/kg b.w./day) promoted 102.22% (young) and 103.45% (elderly) reductions in cyclophosphamide-induced damage in male mice. Botryosphaeran also exerted chemoprotective effects in LDLr-/- and wild-type (C57BL/6) mice. Botryosphaeran treatment for 15 days at a dose of 30 mg/kg b.w./day improved the lipidic profile (reductions of 53.8-84.3%), and decreased aortic lipid deposition (32.8%) in the LDLr-/- atherosclerotic mice. The results indicate botryosphaeran has relevant biologic effects, making it a promising candidate for the development of new therapeutic agents.

Antimutagenic activity of ipriflavone against the DNA-damage induced by cyclophosphamide in mice.

In the present study we evaluated the potential of ipriflavone against the cytotoxic and mutagenic effects induced by cyclophosphamide chemotherapeutic agent in bone marrow cells of mice, using the micronucleus assay in vivo on cells of bone marrow. The study was performed following three protocols: pre-treatment, simultaneous treatment and post treatment. The results demonstrated that ipriflavone has a protective effect against mutagenicity induced by cyclophosphamide in the pre-treatment and post-treatment and against the cytotoxicity in all treatments. There was variation between the genders in some of the experimental groups. To evaluate their possible mechanisms of action, it was performed the DPPH assay, which showed no ability to donate hydrogens, suggesting that it acts through other mechanisms. Due to its ability to prevent chromosomal damage, ipriflavone is likely to open an interest field concerning its possible the use in clinical applications.