*3.2.2 Immunosuppressive*

*Aflatoxin B1 Occurrence, Detection and Toxicological Effects*

and subsequent AFB1 production [17, 18].

**3.2 The toxic effects of AFB1 on human and animals**

the insects and microorganisms in the stored grain are also Factors affecting water activity. It was found to be closely related to climate in the detection of aflatoxin levels after storage of Benin corn. Benin's aflatoxin contamination levels increase in dry and hot conditions in June each year; while the harvest season is affected by climate, the peaks of rainfall or the late planting of corn will increase aflatoxin levels during the rainy season [16]. Limiting the occurrence of AFB1 before crop harvesting can be achieved by reducing drought and temperature, controlling weeds, reducing insect damage, efficient harvesting techniques, and reducing soil Aspergillus spores through crop turnover. Using biological control, a competitive, non-toxigenic strain of Aspergillus flavus is applied to the developing soil to compete with naturally occurring toxigenic strains. Studies have shown that these biological control strategy can aflatoxin. The pollution is reduced by about 80–90%. Control of afb1 sensitive crops after harvest can be achieved by controlling factors that affect fungal growth, such as water activity, temperature, gaseous environment, and the use of pesticides or food preservatives. Harvesting only cereals with a moisture content of around 24% reduces the risk of grain damage

In 1963, Asao et al. completed the structural clarification of AFB1, a member of the aflatoxin family containing a fused difuranyl group [19]. AFB1 is highly toxic to humans and several animals, and has three major characteristics: organophilic, genotoxic, and carcinogenic. Its pro-organism is mainly caused by damage to the liver, which can lead to hepatic hemorrhage and hepatocyte necrosis. The genotoxicity is mainly to induce the formation of AFB1-DNA adduct and the hot spot mutation of P53 gene. The carcinogenicity is mainly caused by hepatocellular carcinoma. The main toxicological effect of AFB1 is to induce DNA damage. AFB1 has been proven to be the main cause of liver cancer in patients with hepatitis B virus infection. It is a genotoxic liver cancer, which may cause cancer by inducing DNA adducts, leading to genetic changes in target cells, leading to DNA strand breaks and DNA base damage. And oxidative damage can eventually lead to cancer. AFB1 is mainly metabolized by the liver, and AFB1 taken from food is mainly metabolized by the cytochrome P450 enzyme to the final carcinogen AFB1-8-9 epoxide (AFBO). When AFBO reacts with DNA, it inhibits gene mutation in P53, a hotspot coding region of exon 249, by interacting with guanine bases, which may lead to HCC. AFB1 is metabolized by the P450 system into a number of hydroxylated products, including AFM1, AFQ1, AFP1, AFB2a [11, 20–25]. After aflatoxin is ingested into the human body, it mainly manifests as an acute or chronic disease. Acute attacks usually involve high concentrations of aflatoxins. For example, 317 cases of acute liver failure occurred in Kenya in 2004. The main reason is the consumption of aflatoxin-contaminated corn, and the case of patients with AFB1 lysine in serum. The adduct concentration was the highest in history. Growth retardation, immunosuppression, and carcinogenicity are chronic effects, and the incidence of chronic attacks in developing countries is higher because of exposure to low levels

An epidemiological survey was conducted in West Africa to measure exposure to aflatoxins in children between 9 months and 5 years of age, and their growth, development and height were examined against the reference population of World Health Organization (WHO) [27]. Studies have shown a strong association between

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of aflatoxin intake [26].

*3.2.1 Effect of aflatoxin on growth and development*

In these animal studies, AFB1 has been shown to induce immunosuppression. For example, in studies of AFB1 exposed animals, it was found that the activity of B cells and T cells decreased, because T cells were more sensitive to AFB1 toxicity [30]. Research data from GY et al. showed that chicken phagocytic cells were severely damaged during aflatoxosis, and the ability to remove foreign substances from the circulation decreased, which may reduce the ability to process antigenic components. Aflatoxell chickens are more susceptible to infection [31]. In pigs, AFB1 exposure reduces lymphocyte response to mitogens, inhibits large phage migration and delayed skin allergic reactions [32]. Although many data on AFB1 immune effects have been obtained from animal studies, there is little data on the effects of long-term consumption of food contaminated with AFB1 on the human immune system. The effect on the immune system by aflatoxins in the diet of Gambian children found a decrease in sIgA levels in saliva, probably due to the high level of exposure to aflatoxins in the diet [33]. In a study of aflatoxin AFB1 exposure and cellular immune status in 64 Ghanaians, it was found that AFB1 exposure may result in a decrease in the major constituent cell T cells and B cells that cause lymphocyte subpopulations. High levels of AFB1 albumin adducts significantly reduced perforin- and granzyme a levels in CD8+ cytotoxic T cells compared to low levels of AFB1 albumin adduct. In participants with high levels of AFB1, changes in these immune parameters may result in impaired cellular immune function, thereby reducing host resistance to infection [34].
