Effect of dietary honey on intestinal microflora and toxicity of mycotoxins in mice

BACKGROUND: Bee honey is a functional food which has a unique composition, antimicrobial properties and bifidogenic effect. In order to assess whether honey can inhibit the toxic effect of mycotoxins, the present study was undertaken. METHODS: Production of biomass and toxins by Aspergillus parasiticus and Aspergillus ochraceus were followed in media without and with honey. Although aflatoxins and ochratoxin A. were administrated to male Swiss albino mice up to 1 μg and 10 ng/kg body weight/day respectively. The experimental animals were fed diets without our with 10% honey for two months. The changes in colonic probiotic bacteria, determintal colon enzyme glucuronidases, and genotoxicity were followed. RESULTS: Addition of 32% in its media increased the biomass of A parasiticus, while the biomass of A. ochraceus decreased and Ochratoxin A. was not produced. When the honey was added at the ratio of 32 and 48% in the medium. No relationship was found between mycelium weight and production of mycotoxins. Oral administration of aflatoxins (mixture of B(1), B(2), G(1) and G(2)) and Ochratoxin A. induced structural and numerical chromosomal aberrations in bone marrow and germ cells of male mice, whereas, honey treatment reduced the genotoxicity of mycotoxins. Also both toxins induced histopathological changes in liver and kidney. Feeding on diet supplemented with honey improved the histopathological changes in case of aflatoxin group, but not in the case of ochratoxin A. group (except of kidney in two cases). No significant differences were found in the activity of colon β-glucuronidase between group fed diet with or without honey. On the other hand, the colon bifido bacteria and lactobacilli counts were increased markedly in group receiving diet supplemented with honey. CONCLUSION: Substituting sugars with honey in processed food can inhibit the harmful and genotoxic effects of mycotoxins, and improve the gut microflora

Herbal Medicine. Toxicity and Recent Trends in Assessing Their Potential Toxic Effects

Herbal medicine has been used for thousands of years. It is estimated that 80% of world population rely on traditional herbal medicine for primary health care. In recent years, herbal remedies have been considered as dietary supplement for disease prevention and as alternative/complementary medicine. A wide variety of herbal medicines are readily available in the market all over the world. With the rising utilisation of herbal products, safety and efficacy of herbal medicine have become a public health concern. Adverse health effects associated with herbal products could be attributed to both inherent toxic effects of herbal medicine and toxicities induced by adulterants/contaminants. Increasing evidence, regarding side effects of herbal medicine, has highlighted the demand and necessity of toxicological studies for herbal products. Toxicology constitutes an essential role in the development of herbal medicines. With the advancements of analytical techniques and molecular technology, coupling with the conventional test systems, the '-omic-' technology makes a significant contribution to the predictive and preclinical toxicology of herbal medicine. In this chapter, side effects related to herbal medicine and its adulterants/contaminants are summarised. The recent application of '-omic-' technology for toxicological evaluation of herbal products is also illustrated. © 2012 Elsevier Ltd.link_to_subscribed_fulltex

Kick-off meeting and report

Deliverable 3.1 ;9 pagesinfo:eu-repo/semantics/publishe

Potential endocrine disrupting effect of ochratoxin A on human placental 3ß-hydroxysteroid dehydrogenase/isomerase in JEG-3 cells at levels relevant to human exposure

Ochratoxin A (OTA) is a common foodborne mycotoxin. Besides its classical toxicities, it is also associated with the impairment of steroidogenesis in rats. It is hypothesized that OTA may act as an endocrine disruptor by intervening 3β-hydroxysteroid dehydrogenase/isomerase (3β-HSD). To address this hypothesis, human placental cells JEG-3 were used in vitro to examine the effects of short- and long-term OTA exposures on expression levels of 3β-HSD1 and progesterone secretion at 24-96. h. Results showed that both cytotoxic and non-cytotoxic levels of OTA induced 3β-HSD1 mRNA expression by 281-378% at 72 and 96. h. A significant induction (43-316%) of 3β-HSD1 protein expression was observed at 48, 72 and 96. h, and the progesterone production with the involvement of 3β-HSD1 was significantly increased by 22-89% after 48-96. h. This is the first study to demonstrate OTA up-regulates 3β-HSD1 expression in human placental cells, indicating the potential endocrine-disrupting property of OTA

A new research agenda will be developed to address the gaps in knowledge and the next steps in coordination might be planned

Deliverable D3.5 ;16 pagesinfo:eu-repo/semantics/publishe

Intestinal Mucus Alters the Ability of Probiotic Bacteria To Bind Aflatoxin B(1) In Vitro

Several probiotics are known to bind aflatoxin B(1) (AFB(1)) to their surfaces and to adhere to intestinal mucus. In this study, preincubation of two probiotic preparations with either AFB(1) or mucus reduced the subsequent surface binding of mucus and AFB(1), respectively, in a strain-dependent manner

Surface Binding of Aflatoxin B(1) by Lactic Acid Bacteria

Specific lactic acid bacterial strains remove toxins from liquid media by physical binding. The stability of the aflatoxin B(1) complexes formed with 12 bacterial strains in both viable and nonviable (heat- or acid-treated) forms was assessed by repetitive aqueous extraction. By the fifth extraction, up to 71% of the total aflatoxin B(1) remained bound. Nonviable bacteria retained the highest amount of aflatoxin B(1). Lactobacillus rhamnosus strain GG (ATCC 53103) and L. rhamnosus strain LC-705 (DSM 7061) removed aflatoxin B(1) from solution most efficiently and were selected for further study. The accessibility of bound aflatoxin B(1) to an antibody in an indirect competitive inhibition enzyme-linked immunosorbent assay suggests that surface components of these bacteria are involved in binding. Further evidence is the recovery of around 90% of the bound aflatoxin from the bacteria by solvent extraction. Autoclaving and sonication did not release any detectable aflatoxin B(1). Variation in temperature (4 to 37°C) and pH (2 to 10) did not have any significant effect on the amount of aflatoxin B(1) released. Binding of aflatoxin B(1) appears to be predominantly extracellular for viable and heat-treated bacteria. Acid treatment may permit intracellular binding. In all cases, binding is of a reversible nature, but the stability of the complexes formed depends on strain, treatment, and environmental conditions