Anti-Aflatoxin monoclonal antibody, clone BTB2

Hepatocellular carcinoma (HCC) is the fifth most commonly diagnosed cancer worldwide and is associated with poor prognosis. The current study aimed to assess the therapeutic efficacy of resveratrol when administered alone and in combination with nicotinamide against alcohol-aflatoxin B1-induced HCC. Results reveal that during the development and progression of cancer, there was a decline in the level of antioxidant enzymes catalase, glutathione peroxidase, glutathione reductase (GR), antioxidant glutathione, and glutathioneS-transferase, which is an enzyme of detoxification pathways. Treatment of resveratrol restored the level of catalase and glutathione peroxidase toward normal in alcohol-aflatoxin B1-induced HCC; however, nicotinamide worked in concert with resveratrol only in upregulating the activity of glutathione reductase, glutathione level, and glutathioneS-transferase. SIRT1 agonist resveratrol was observed to modulate the activity of antioxidant enzymes by negatively regulating the expression of nuclear factor-kappa B (NF-kappa B) in alcohol-aflatoxin B1-induced HCC, thereby suggesting a cross-talk between antioxidant enzymes SIRT1 and NF-kappa B during the development and progression of HCC and its therapeutics by resveratrol and nicotinamide.

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.