385
Aflatoxins-Induced Inflammatory Responses
It has been observed that AFB1 decreased the expression of IL-4 expression (antiinflammatory) but increased the expression of IFN-γ and TNF-α (pro-inflammatory
cytokines) form natural killer cells [22]. These findings indicated that AF-B1 exposure potentiated the inflammatory responses by regulating the cytokines related
genes expression. Moreover, AFB1 interrupted the process of the antigen- presenting
capacity of porcine dendritic cells. It may be a possible mechanism behind AF-B1induced immunotoxicity [23]. It has also been reported that AFs exposure decreased
the efficiency of immunization in children and made them susceptible to infections [30].
Aflatoxins-Induced Lipid Metabolism
The liver is considered as a target organ for AFs toxicity accompanied by dyslipidemia. Dyslipidemia may happen owing to altered expression of lipid and lipoprotein
metabolizing genes [26]. Literature has shown that plasma dyslipidemia due to
AFB1 exposure was characterized by an elevated level of cholesterol, free fatty
acids, and triglyceride with a reduced level of phospholipids and HDL 3 –cholesterol.
On the other hand, hepatic dyslipidemia after AFB1 exposure was characterized by
an elevated level of cholesterol, phospholipids, and triglyceride. Additionally,
expression of all 5 lipid-related genes was significantly changed after AF-B1 exposure [27]. In DM, glucose loss due to deficiency of insulin enhances the demand for
lipid oxidation for the purpose of energy metabolism and the key mechanism working behind it is β-oxidation of fatty acids [31]. Fatty acids beta-oxidation comprises
of multi-steps in which fatty acids are processed to produce acyl-CoA which enter
TCA cycle. It has been observed that AFs exposure to diabetic rats significantly
reduced the expression of two important fatty acid β-oxidation enzymes named 17
β-hydroxysteroid dehydrogenase-IV and trifunctional enzyme subunit alpha [32].
Another study proved that AFs exposure caused the lipid metabolism disorders in
addition to the increased gluconeogenesis in rat liver [26].
Strategies to Control Aflatoxin
It is needed to control AFs exposure at all stages from field to dining table in order
to reduce the risk of health hazards. Pre-harvest approaches include practicing targeted plant breeding, improving the host plant resistance, and usage of various biological control methods. Pre-harvesting techniques may be followed by
post-harvesting techniques for better control, including appropriate drying, processing, and storage of susceptible crops. It is a rationale to make arrangements for
23 Role of Aflatoxins as EDCs in Metabolic Disorders
Aflatoxins-Induced Inflammatory Responses
It has been observed that AFB1 decreased the expression of IL-4 expression (antiinflammatory) but increased the expression of IFN-γ and TNF-α (pro-inflammatory
cytokines) form natural killer cells [22]. These findings indicated that AF-B1 exposure potentiated the inflammatory responses by regulating the cytokines related
genes expression. Moreover, AFB1 interrupted the process of the antigen- presenting
capacity of porcine dendritic cells. It may be a possible mechanism behind AF-B1induced immunotoxicity [23]. It has also been reported that AFs exposure decreased
the efficiency of immunization in children and made them susceptible to infections [30].
Aflatoxins-Induced Lipid Metabolism
The liver is considered as a target organ for AFs toxicity accompanied by dyslipidemia. Dyslipidemia may happen owing to altered expression of lipid and lipoprotein
metabolizing genes [26]. Literature has shown that plasma dyslipidemia due to
AFB1 exposure was characterized by an elevated level of cholesterol, free fatty
acids, and triglyceride with a reduced level of phospholipids and HDL 3 –cholesterol.
On the other hand, hepatic dyslipidemia after AFB1 exposure was characterized by
an elevated level of cholesterol, phospholipids, and triglyceride. Additionally,
expression of all 5 lipid-related genes was significantly changed after AF-B1 exposure [27]. In DM, glucose loss due to deficiency of insulin enhances the demand for
lipid oxidation for the purpose of energy metabolism and the key mechanism working behind it is β-oxidation of fatty acids [31]. Fatty acids beta-oxidation comprises
of multi-steps in which fatty acids are processed to produce acyl-CoA which enter
TCA cycle. It has been observed that AFs exposure to diabetic rats significantly
reduced the expression of two important fatty acid β-oxidation enzymes named 17
β-hydroxysteroid dehydrogenase-IV and trifunctional enzyme subunit alpha [32].
Another study proved that AFs exposure caused the lipid metabolism disorders in
addition to the increased gluconeogenesis in rat liver [26].
Strategies to Control Aflatoxin
It is needed to control AFs exposure at all stages from field to dining table in order
to reduce the risk of health hazards. Pre-harvest approaches include practicing targeted plant breeding, improving the host plant resistance, and usage of various biological control methods. Pre-harvesting techniques may be followed by
post-harvesting techniques for better control, including appropriate drying, processing, and storage of susceptible crops. It is a rationale to make arrangements for
23 Role of Aflatoxins as EDCs in Metabolic Disorders