|Year : 2017 | Volume
| Issue : 3 | Page : 60-63
Bioprospecting of Medicinal Plants for Detoxification of Aflatoxins
Department of Crop Sciences, College of Agricultural and Marine Sciences, Sultan Qaboos University, Al-Khodh, Muscat, Sultanate of Oman
|Date of Web Publication||4-Jul-2017|
Department of Crop Sciences, College of Agricultural and Marine Sciences, Sultan Qaboos University, PO Box-34, Al-Khodh, Muscat 123
Sultanate of Oman
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Aflatoxin contamination of foods is a major concern worldwide as aflatoxin B1 is implicated in the etiology of hepatic cancer in humans. The aflatoxins are a group of secondary metabolites mainly produced by Aspergillus flavus and Aspergillus parasiticus when they grow on a wide range of agricultural commodities. Once the food commodities are contaminated with aflatoxin, removal of the toxin is extremely difficult as the toxin is highly stable. Several approaches for detoxification of aflatoxins have been proposed; however, each method has its own shortcomings. Natural plant products are of interest as a source of safe and alternative way for detoxification of aflatoxins. This paper summarizes some of the recent developments in the detoxification of aflatoxins by using plant products.
Keywords: Aflatoxin, Aspergillus flavus, detoxification, medicinal plants
|How to cite this article:|
Velazhahan R. Bioprospecting of Medicinal Plants for Detoxification of Aflatoxins. Int J Nutr Pharmacol Neurol Dis 2017;7:60-3
|How to cite this URL:|
Velazhahan R. Bioprospecting of Medicinal Plants for Detoxification of Aflatoxins. Int J Nutr Pharmacol Neurol Dis [serial online] 2017 [cited 2020 Jun 2];7:60-3. Available from: http://www.ijnpnd.com/text.asp?2017/7/3/60/209424
| Introduction|| |
Aflatoxins are a group of structurally related, acutely toxic, carcinogenic, mutagenic, teratogenic, and immunosuppressive secondary metabolites produced predominantly by certain strains of Aspergillus flavus and Aspergillus parasiticus. Aflatoxins were discovered after the outbreak of “Turkey X disease” in 1960 in England, which resulted in the mortality of approximately 100,000 turkey poults. This outbreak was attributed to consumption of mold-contaminated peanut meal. The fungus present in the contaminated peanut meal was identified as A. flavus and the toxic metabolite produced by the fungus was named as “aflatoxin” indicating the first letter from “Aspergillus” and the first three letters from “flavus”. Aflatoxin contamination occurs on a wide variety of agricultural commodities, including peanut, corn, pistachio nut, rice, wheat and spices like chili, black pepper, and turmeric, that are commonly used for human consumption.
Currently 18 different types of aflatoxins have been identified among which aflatoxin B1 (AFB1), B2 (AFB2), G1 (AFG1), and G2 (AFG2) are frequently found in food. The letters “B” and “G” refer to the color of the fluorescent emissions under ultraviolet light (B for Blue; G for Green) and the numbers 1 and 2 refer to their relative mobility in thin-layer chromatography on silica gel. A. flavus produces AFB1 and AFB2, whereas A. parasiticus produces AFB1, AFB2, AFG1, and AFG2. Toxigenic cells export these metabolites by way of exocytosis. Approximately 30 genes are involved in the aflatoxin biosynthesis and are clustered in a 75-kb deoxyribonucleic acid (DNA) region of A. flavus and A. parasiticus.
| Impact of Aflatoxins on Human and Animal Health|| |
Chemically, aflatoxins are difurocoumarolactones (difurocoumarin derivatives). Their structure comprises of a bifuran ring fused to a coumarin nucleus with a pentenone ring (in B aflatoxins), or a six-membered lactone ring (in G aflatoxins). Consumption of aflatoxin contaminated food and feed leads to the disease called “aflatoxicosis” in livestock, domestic animals, and humans. Aflatoxicosis is recognized as the sixth amongst the 10 most important health risks identified by World Health Organization (WHO) for developing countries. Among the aflatoxins, AFB1 is the most prevalent and dangerous mycotoxin to humans and considered as one of the most potent hepatocarcinogens known. Aflatoxin has been proven to also be genotoxic and neurotoxic in test animals. In humans and susceptible animals, cytochrome P450 enzymes convert AFB1 to AFB1-exo-8,9-epoxide, a reactive form that binds to DNA and proteins resulting in mutation and oxidative damage to various macromolecules. AFB1 metabolites bind with albumin and form aflatoxin-serum albumin adducts. This aflatoxin-adduct in the peripheral blood is used as a biomarker to measure aflatoxin exposure in humans. AFB1 metabolites react with guanine residues in the DNA, resulting in (AFB1)-N7-guanine adducts. AFB1 induces transversion of G to T at codon 249 of the p53 tumor suppressor gene, which has been strongly associated with hepatocellular carcinoma. The International Agency for Research on Cancer classified the AFB1 as class I human carcinogens.
When AFB1 contaminated feed is ingested by dairy cattle, it is transformed into aflatoxin M1 in the body of the animal through enzymatic hydroxylation of AFB1 at the 9a-position and secreted in milk. In case of poultry, the presence of AFB1 residues in the meat and eggs of poultry birds fed with aflatoxin contaminated feed has been reported. Aflatoxins have been detected in the blood of pregnant women, in neonatal umbilical cord blood, and in breast milk. Hence, the presence of aflatoxins in the food chain threatens people’s livelihood, agricultural development, food security, and human health.
Aflatoxin contamination of food commodities occurs by colonization of aflatoxigenic fungi on susceptible crops in the field under suitable temperature and humidity conditions or during harvesting, drying, storage, or processing. The aflatoxins are extremely durable under most conditions of storage, handling, and processing of foods or feeds. Hence many countries have established regulations regarding the permissible level of aflatoxins in foods and feeds. The US Food and Drug Administration has set an aflatoxin tolerance limit of 20 parts per billion (ppb) for foods and for most feeds and feed ingredients. The European Union has enacted very severe aflatoxin tolerance level for AFB1 and total aflatoxins in nuts and cereals for human consumption at 2 and 4 ppb, respectively. Due to such restrictions, aflatoxin contamination of agricultural commodities is not only a serious food safety concern, but has significant economic implications for the agricultural industry.
| Detoxification of Aflatoxins|| |
Eradication or removal of aflatoxin after its formation in a commodity is very difficult since the toxin is highly stable. Hence, current aflatoxin management strategies are primarily aimed at reducing infection and colonization of aflatoxigenic fungi on agricultural commodities. These include breeding for aflatoxin resistance, development of good agricultural practices, biological control of aflatoxigenic fungi, and improved storage methods. If aflatoxin contamination occurs in agricultural commodities even after following the above management strategies, postharvest decontamination/detoxification procedures can be employed to remove or reduce the level of toxins in foods and feeds.
In the case of feeds, sequestering or binding agents are widely used for mixing with aflatoxin-contaminated feed to reduce or prevent exposure of farm animals to aflatoxins. The sequestering agents tightly bind to the aflatoxins present in the contaminated feed without disassociating in the gastrointestinal tract of the animals and the toxin-binder complex then passes harmlessly through the animal and eliminated via the feces.
| Botanicals in Aflatoxin Detoxification|| |
Several physical, chemical, and biological methods have been developed for detoxification of aflatoxins. However, each treatment has its own limitations, as the treated product should be safe and the nutrient contents of the treated product should not be reduced. Several researchers reported the use of medicinal plants for detoxification of aflatoxins. Aqueous extract of Ajowan (Trachyspermum ammi) seeds was reported to have an aflatoxin inactivation factor and treatment of aflatoxin with the aqueous extract of Ajowan seeds showed an approximately 80% reduction in total aflatoxin content over the control. In another study, dialyzed extract of T. ammi seeds was found effective in degrading >90% of the AFG1 and the aflatoxin detoxifying activity of the extract was drastically reduced upon boiling at 100°C for 10 min. The degradation of other aflatoxins, namely, AFB1 (61%), AFB2 (54%), and AFG2 (46%) by the dialyzed T. ammi extract was also reported. Modification of lactone ring structure of AFG1 was suggested as the mechanism of detoxification based on the analysis of the degradation products of AFG1 by mass spectrometry. Analysis of the biological toxicity of the degradation products of AFG1 by testing their ability to induce chromosomal aberration in corn revealed that AFG1 caused more than 2% chromosomal aberration at 40 ppm concentration, whereas AFG1 after treatment with T. ammi extract failed to induce chromosomal aberration.
The potential of leaf extract of Zimmu, an interspecific hybrid of Allium sativum and Allium cepa, in detoxification of AFB1 has been documented. An aqueous extract from leaves of Vasaka (Adhatoda vasica) has been shown to detoxify AFB1 (≥98%) when incubated for 24 h at 37°C. The detoxification of AFB1 by A. vasica extract was confirmed by liquid chromatography–mass spectrometry (LC–MS) analysis. Analysis of the A. vasica leaf extract revealed the presence of high molecular weight (nondialyzable), water-soluble and thermolabile aflatoxin detoxification principle(s) in the extract. Kannan and Velazhahan reported that aflatoxins could be degraded by methanolic extract (1%) obtained from leaves of Barleria lupulina. The highest percentage detoxification values of 61.1, 71.4, 94.4, and 58.8% for AFB1, AFB2, AFG1, and AFG2, respectively, were reported at pH 10. It was demonstrated that the aqueous extract obtained from the leaves of Ocimum basilicum was highly effective in degrading AFB1 and AFB2 and showed degradation of 90.4 and 88.6%, respectively. The structural elucidation of degraded products of the toxins by LC–MS/MS revealed removal of double bond in the terminal furan ring and modification of lactone group, indicating less toxicity as compared to their parent compound.
Several phytochemicals or plant products have been shown to have ameliorative effects against AFB1-induced toxicity in animals. Garlic extract was shown to prevent AFB1-induced carcinogenesis in the toad (Bufo regularis). Administration of Thonningia sanguinea extract (5 ml/kg) intraperitoneally to rats before AFB1 treatment significantly reduced the liver injury induced by AFB1. The reversal of toxigenic effects of AFB1 by alcoholic extract of African nutmeg (Monodora myristica) on cockerels was demonstrated. Pretreatment of rats with a compound (dimethyl-4,4′dimethoxy-5, 6, 5′,6′-dimethylenedioxy biphenyl-2,2′-dicarboxylate) isolated from a Chinese herb was shown to inhibit liver damage caused by AFB1. Farombi et al. reported on the potential of kolaviron, a natural biflavonoid of Garcinia kola seeds in prevention of AFB1-induced genotoxicity and hepatic oxidative damage in rats. de Boer et al. demonstrated that addition of Huang-qin (Scutellaria baicalensis) powder (1%) to the feed of rats reduced the mutant frequency induced by subsequent administration of AFB1 by approximately 60 to 77%. Brinda et al. demonstrated that pre-feeding of Wistar rats with a spray-dried formulation of A. vasica leaf extract counteracted the hepatic dysfunction induced by subsequent treatment with AFB1. Dietary addition of 1% black seed (Nigella sativa) or Ceylon cinnamon (Cinnamomum verum) was found to alleviate the toxic effects of AFB1 in fish (Oreochromis niloticus). Oral administration of 2% aqueous black tea extract has been reported to ameliorate aflatoxin-induced lipid peroxidation in the liver of mice. Recently, Linardaki et al. demonstrated that pretreatment of adult mice with saffron (Crocus sativus) prevents learning/memory defects and neurobiochemical alterations induced by subsequent exposure to AFB1.
| Conclusions|| |
Recently, studies on the effect of A. vasica on growth performance and biochemical parameters in serum and liver of broiler chicks demonstrated that feed intake and body weight gain were not significantly affected by dietary supplementation of A. vasica leaf powder up to 1.5% level when compared with the control feed. No significant differences were observed in the levels of hemoglobin, red blood cells, packed cell volume, glucose, and cholesterol in the serum of broiler chickens due to dietary supplementation of A. vasica powder. Such medicinal plants may be ideal choice for development of functional foods or biologically safe herbal feed additives to reduce the toxic effects of aflatoxin in feeds.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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