The toxic effects of aflatoxins appear sometime prior to ingestion in diet. These effects can be observed as impairment of biomarkers in animals including reduced daily feed intake (FI), daily growth rate (GR), feed conversion efficiency (FCE) and packed-cell-volume (PCV)
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(Medina et al., 2014). Others impairments are maladjusted levels of serum proteins mainly total proteins, albumin, globulin and albumin/globulin ratio (AGR) as well as defective relative weights of liver, kidney and spleen associated with histopathological changes of internal organs such as liver, kidney and spleen (Rotimi et al., 2018). Various reports show that dietary aflatoxins in various animals reduce FI as observed in broilers (Yang et al., 2012), white shrimps (Salazar et al., 2012) and quail (Mahmood et al., 2017).
Dietary aflatoxins have detrimental effects on FCE and GR. Yang et al. (2012) and Nasrabadi et al. (2013) reported that impairment of FCE and GR is caused by reduced ratio of villus height to the intestinal crypt depth in the intestine which decreases with increasing aflatoxin contamination of diets and diminish nutrient absorption from the gut (Applegate et al., 2009). It has been reported that dietary aflatoxins reduce value of PCV and favour increase of serum globulin level at the expense of albumin and diminish AGR (Kaneko et al., 2008 cited by Dónmez et al., 2012). However, susceptibilities of different groups of animals to the toxic effects of aflatoxins are caused by different forms of the enzymes such as cytochrome P450s, glutathione and S-transferases that metabolize aflatoxins (Dohnal et al., 2014). Chronic aflatoxicosis which is a more noxious form in animals, appears in various types of toxicity as negative health impacts; explained here in relation to animal health and production.
(i) The AFB1 adducts
This is a reaction of AFB1 and DNA or RNA forming AFB1-DNA and AFB1-RNA adducts (Muhammad et al., 2019). These can inhibit transcription and translation, to cause DNA mutation, carcinogenesis and other conditions detrimental to animal health. Through a series of reactions, AFB1 can produce adducts with lysine residues in proteins which then can cause toxicity through impairment of protein synthesis and function the vital organs (Wogan et al., 2012).
(ii) Mutagenicity
This is a detrimental effect of AFB1 caused by binding of AFB1 to hepatic DNA and form mutation in liver DNA (Feddern et al., 2013). Aflatoxins are mutagenic in the sense that the effect leads to mutation of genetic code and cause DNA alteration and breakage of chromosome, gene rearrangements and malformation of genetic information (Woo et al., 2011). This condition has great impacts leading to many health challenges which can occur in all animals and in humans.
15 (iii) Hepatotoxicity and nephrotoxicity
Hepatotoxicity is a condition of toxicity in liver characterised by increased relative weight and pale or yellow pigmentation of liver which also becomes soft and friable (Hinton et al., 2003). Chronic exposure of AFB1 that may combine with hepatitis-B infections is likely to result into liver cancer. Activation of liver by AFB1 may result into the hepatotoxicity commonly known as hepatocellular carcinoma. Similarly, aflatoxins may cause nephrotoxicity which is a toxicity condition in kidneys brought about by accumulation of any potent toxic agent in the renal tubules (Devendran et al., 2011).
(iv) Immunotoxicity
This is impairment of immune system of an animal and humans by a toxic agent leading to reduced body immunity. Poultry which is highly vulnerable to aflatoxicosis encounter immune-toxicity very easily. Birds depend on the bursa of Fabricius, thymus and spleen to produce leukocytes for active immunity (Hinton et al., 2003). It is reported that even at low level of dietary aflatoxins these organs are likely to be challenged and injured and lower immunity of the birds. The mechanism of aflatoxin immunotoxicity is not clearly known. However, according to Mehrzad et al. (2014), the AFB1 can quickly impair the phagocytic capacity of dendritic cells, up-regulating the membrane expression levels of dendritic cell activation markers and lead to poor T-cell stimulatory capacity.
(v) Intestinal toxicity
The intestinal toxicity occurs as a result of AFB1 lowering the size (length/weight) of the duodenum and jejunum (Yunus et al., 2011) and affect tissue morphology. Particularly in chickens, AFB1 has been shown to raise crypt depth in the jejunum, decrease villus height in the duodenum, then reduce the ratio between villus height/crypt depth in all three parts of the small intestine and reduce feed efficiency and growth (Yang et al., 2012).
(vi) Embryo toxicity
The effect of embryonic exposure to toxins has been proved to be risky to poultry embryo. AFB1 and its metabolites can be transferred from contaminated diet ingested by laying hen into the albumen and yolk of the egg as AFM1 (Çelik et al., 2000; Devendran et al., 2011). The AFB1 is hydroxilated into AFM1 in the liver by hepatic microsomal cytochrome P450
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enzyme family (Battacone et al., 2009; Britzi et al., 2013). The AFM1 is a common metabolite detected in milk, eggs and meat. Though not as carcinogenic as AFB1, the AFM1 can cause acute toxicity in developing embryos (Çelik et al., 2000).
(vii) Production losses
Aflatoxins, particularly AFB1, negatively affect production values and result into economic losses in livestock industry, particularly in poultry. The adverse production effects are observed as low weight gain, reduced feed intake and reduced feed conversion efficiency (Thieu et al., 2008). However, these parameters abnormally may vary with type of animals and probably modality of feeding and dietary balance. For instance studies showed that AFB1 contaminated diet resulted into reduced feed intake and weight gain in chicken and turkeys without effect on feed conversion efficiency (Applegate et al., 2009; Devendran et al., 2011).
2.3 Aflatoxin biosynthesis and contamination of crops and feeds