Pathological Role of Oxidative Stress in Aflatoxin-Induced Toxicity in Different Experimental Models and Protective Effect of Phytochemicals: A Review.
Martha Cebile JobeDoctor Mziwenkosi Nhlanhla MthiyanePhiwayinkosi Vusi DludlaSithandiwe E Mazibuko-MbejeDamian C OnwudiweMulunda MwanzaPublished in: Molecules (Basel, Switzerland) (2023)
Aflatoxin B1 is a secondary metabolite with a potentially devastating effect in causing liver damage in broiler chickens, and this is mainly facilitated through the generation of oxidative stress and malonaldehyde build-up. In the past few years, significant progress has been made in controlling the invasion of aflatoxins. Phytochemicals are some of the commonly used molecules endowed with potential therapeutic effects to ameliorate aflatoxin, by inhibiting the production of reactive oxygen species and enhancing intracellular antioxidant enzymes. Experimental models involving cell cultures and broiler chickens exposed to aflatoxin or contaminated diet have been used to investigate the ameliorative effects of phytochemicals against aflatoxin toxicity. Electronic databases such as PubMed, Science Direct, and Google Scholar were used to identify relevant data sources. The retrieved information reported on the link between aflatoxin B1-included cytotoxicity and the ameliorative potential/role of phytochemicals in chickens. Importantly, retrieved data showed that phytochemicals may potentially protect against aflatoxin B1-induced cytotoxicity by ameliorating oxidative stress and enhancing intracellular antioxidants. Preclinical data indicate that activation of nuclear factor erythroid 2-related factor 2 (Nrf2), together with its downstream antioxidant genes, may be a potential therapeutic mechanism by which phytochemicals neutralize oxidative stress. This highlights the need for more research to determine whether phytochemicals can be considered a useful therapeutic intervention in controlling mycotoxins to improve broiler health and productivity.
Keyphrases
- oxidative stress
- diabetic rats
- reactive oxygen species
- dna damage
- induced apoptosis
- ischemia reperfusion injury
- nuclear factor
- big data
- public health
- electronic health record
- randomized controlled trial
- healthcare
- toll like receptor
- heat stress
- genome wide
- heavy metals
- single cell
- drug induced
- stem cells
- immune response
- human health
- artificial intelligence
- endothelial cells
- stress induced
- bone marrow