Abstract
Uganda is an agrarian country where farming employs more than 60% of the population. Aflatoxins remain a scourge in the country, unprecedentedly reducing the nutritional and economic value of agricultural foods. This review was sought to synthetize the country's major findings in relation to the mycotoxins' etiology, epidemiology, detection, quantification, exposure assessment, control, and reduction in different matrices. Electronic results indicate that aflatoxins in Uganda are produced by Aspergillus flavus and A. parasiticus and have been reported in maize, sorghum, sesame, beans, sunflower, millet, peanuts, and cassava. The causes and proliferation of aflatoxigenic contamination of Ugandan foods have been largely due to poor pre-, peri-, and postharvest activities, poor government legislation, lack of awareness, and low levels of education among farmers, entrepreneurs, and consumers on this plague. Little diet diversity has exacerbated the risk of exposure to aflatoxins in Uganda because most of the staple foods are aflatoxin-prone. On the detection and control, these are still marginal, though some devoted scholars have devised and validated a sensitive portable device for on-site aflatoxin detection in maize and shown that starter cultures used for making some cereal-based beverages have the potential to bind aflatoxins. More efforts should be geared towards awareness creation and vaccination against hepatitis B and hepatitis A to reduce the risk of development of liver cancer among the populace.
Highlights
Aflatoxin (AF) is a portmanteau combining “a” for the Aspergillus genus, “fla” for the species flavus, and toxin for poison [1,2,3]. e discovery of aflatoxins traces back to 1960 in which a severe outbreak of Turkey “X” disease was recorded in England with more than 100,000 turkeys, 20,000 ducklings, pheasants, chicks, and partridge poults reported to have died from the calamitous incident [4]. e cause was reported to be due to a series of fluorescent compounds in a peanut meal imported from South America (Brazil) that was served to the poults [5]
The disease syndrome was reported in domesticated animals outside Great Britain. e causative mold, Aspergillus flavus, was isolated from a meal later related to a hepatic problem in ducklings in Uganda [6]. e early history of the Turkey “X” disease outbreak in Great Britain was described in sufficient details by Blount [4, 7], and the toxicity recorded in various animal species was recapitulated by Allcroft [8]
Balikuddembe, Nakasero, Kireka, and Kalerwe had a mean total AF of 7.6 ± 2.3 μg/kg with approximately 20% of the samples having higher than 10 μg/kg statutory AF limit while 45% of household samples had total AF above compliance limit. e AF results from the immunosensor reportedly correlated with high-performance liquid chromatography (HPLC) and enzyme-linked immunosorbent assay (ELISA) results with correlation coefficients of 0.94 and 0.98, respectively [64]
Summary
Ey display potency of toxicity, carcinogenicity, and mutagenicity in the order: AFB1 > AFM1 > AFG1 > AFB2 > AFM2 > AFG2 as exemplified by their lethal dose that causes the death of 50% of subjects (LD50 values) being 0.1–50 mg/kg body weight for most animal species and
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