Anti-Aflatoxin B1-DNA Adduct monoclonal antibody, clone 7B11

To investigate the effects of oral administration of probiotics consortium on lipid metabolism in aflatoxin B1 (AFB1) exposed rats, ninety female albino rats were first grouped into two: NC (control fed standard feed) and AF (fed AFB1-contaminated feed at 40 ppb). After eight weeks, baseline animals were sacrificed from both groups while the others further divided into four groups - NC treated with and without the probiotics consortium, aflatoxin treated with and without the probiotics consortium (NCT, NCC, AFT, and AFC respectively). Five animals from each group were sacrificed weekly for four weeks, with the collection of blood, liver, brain, and the small intestine. Administration of probiotics instigated significant (p < 0.05) reductions in the elevated plasma and organ lipids as well as HDL-TAG and VLDL + LDL CHO concentrations of animals exposed to AF. AF-induced hepatic lipogenesis and up-regulation of 3-hydroxy-3-methylglutaryl-CoA reductase activity were also significantly (p < 0.05) attenuated following treatment with probiotics in a time-dependent manner. Moreover, neither AF nor probiotics had any effect on glycerol-3-phosphate acyltransferase. Lipid peroxidation was significantly (p < 0.05) reduced in probiotics-treated AF groups, compared to the AF-control groups. This study indicates that the probiotic consortium used synergistically ameliorated the AFB1-induced disruptions in lipid metabolism.

The antifungal and aflatoxin B-1(AFB(1)) inhibitory effect of chemically characterisedCallistemon lanceolatusessential oil (CLEO), chitosan nanoparticles, and CLEO loaded chitosan nanoparticles (CLEO-ChNPs) were investigated. Scanning electron microscope observation exhibited the spherical shape of prepared CLEO-ChNPs with an average range of 20-70 nm. Anin-vitrorelease study revealed the controlled volatilisation of CLEO from CLEO-ChNPs. The CLEO-ChNPs caused complete inhibition of growth (4.5 mu l/ml) and AFB(1)(4.0 mu l/ml) production byA. flavusat a low dose compared to free CLEO (5.0 mu l/ml). The antifungal and AFB(1)inhibitory toxicity of CLEO-ChNPs were elucidated using biochemical (effect on ergosterol biosynthesis, membrane cations, mitochondrial membrane potential, C-sources utilisation and cellular methylglyoxal level) and in-silico (interaction with the gene product Erg 28, Cytochrome c oxidase subunit Va, Omt-A, Ver-1, and Nor-1) approaches.