**5. Effect of aflatoxins on the immune system**

glutamate-oxaloacetate and pyruvate transaminases and alkaline phosphatase in rats attrib‐ uted to by the aflatoxins and their metabolites as well as the generated ROS. There was in‐ duced aggregation and loss of chromatin, mitochondrial degeneration and loss of microvilli

Aflatoxin especially AFB has been reported to interfere with the functioning of the various en‐ docrine gland by disrupting the enzymes and their substrates that are responsible for the syn‐ thesis of the various hormones. Aflatoxins and their metabolites as well as the generated ROS have been reported to cause various cancers in different endocrine glands like pituitary gland, granulosa cell tumors of the ovary and adenomas and adenocarcinomas of the adrenal gland, kidneys, thyroid gland, ovaries, testes, thyroid gland, parathyroid glands and endocrine pan‐ creas [4, 90, 108]. The plasma testosterone and luteinizing hormone (LH) concentrations have been reported to reduce in aflatoxin-fed birds [90]. In laboratory animals, aflatoxin causes de‐ layed maturation of both males and females [4, 22, 90, 109]. Aflatoxicosis in white leghorn males chicken decreased feed consumption, body weight, testes weight and semen volume

In humans exposed to chronic aflatoxin-contaminated foods, it has been reported that high‐ er concentrations of aflatoxins occur in the semen of infertile men [3]. It is also associated with low birth weight, a risk factor for jaundice in infants as well as presence of AFM in ma‐ ternal breast milk where it can cause deleterious effect in the newborns [102]. In Nigeria, about 37% of the infertile men had aflatoxin in their blood and semen hence contributing to the incidence of infertility in Nigerians [110]. Experimental results indicate that certain agents like aflatoxins can interfere with the reproductive capabilities of sexes, causing sterili‐ ty, infertility, and abnormal sperm, low sperm count, and/or affect hormone activity in ani‐ mals. Aflatoxins have been reported to disrupt the reproductive system in both male and female animals after ingestion of aflatoxin-contaminated foods. Aflatoxins also cause patho‐ logical alterations in the form of coagulative necrosis especially in the growing and mature follicles and decrease in number and size of graffian and growing follicles with increased number of atretic follicles and small areas of degenerative changes in experimental animals [111]. AFB1 has been reported to have a deleterious effect on the reproductive capacity of laboratory and domestic female animals where they cause reductions in ovarian and uterine sizes, increases fetal resorption, implantation loss and intra-uterine death in the aflatoxin ex‐ posed female rats [111]. They also cause a reduction in the primary spermatocytes and sper‐ matids [112] and affect the morphology of the sperm cells produced [113]. Stillbirths were reported in the 15th to the 18th days of pregnancy in rats [108]. The levels of plasma testos‐ terone, plasma 5a-DHT and absolute and relative testes weights were reported in experi‐ mental animals of aflatoxin-treated males remained low in all age groups and a delay in the onset of sexual maturation during aflatoxicosis [114]. In cows, aflatoxins affected the repro‐

induced by AFB1 in cultured kidney cell lines [24, 85].

(Sharlin et al., 1980) and decreased plasma testosterone values [22].

**4.9. Effect of aflatoxins on the reproductive system**

**4.8. Effect of aflatoxins on the endocrine system**

254 Aflatoxins - Recent Advances and Future Prospects

Chronic consumption of aflatoxin-contaminated foods has been reported to cause immuno‐ suppression in both humans and animals worldwide [7, 89]. In human, aflatoxins affect both the cellular and humoral immune responses where they alter immunological parameters in participants with high AFB1 levels resulting in impairments in cellular immunity hence de‐ creasing the host resistance to infections [115-117]. Aflatoxin exposure has been shown to cause immune suppression, particularly in cell-mediated responses [115-117]. Chronic expo‐ sures of the individual to aflatoxins depress the phagocytic efficiency of the phagocytes and the delayed hypersensitivity reactions in birds [24]. Aflatoxins also deplete the cell popula‐ tions of the thymus; reduce the bone marrow and the red and white blood cells count, mac‐ rophage numbers and the phagocytic activity of the cells [24]. It also depresses the T-celldependent functions of splenic lymphocytes in mice. The natural killer cell function of the peripheral blood lymphocytes are also affected by aflatoxins especially AFB1 [24]. A reduc‐ tion in the leukocyte immunophenotypes in peripheral blood, CD4+ T cell proliferative re‐ sponse, CD4+ T and CD8+ T cell cytokine profiles and monocyte phagocytic activity were reported. Children in developing countries appear to be naturally exposed to aflatoxin through their diet at levels that compromise the immune system. In general, the proportion of childhood growth stunting is directly correlated with the proportion of the population living below the national poverty line and is inversely correlated with gross domestic prod‐ uct per capita [7, 45]. As is the case with liver cancer, childhood stunting is prominent in re‐ gions such as Southeast Asia and Sub-Saharan Africa, where aflatoxin exposure through consuming contaminated food is common [7, 45]. It has been reported that the immunosup‐ pression and nutritional effects of chronic aflatoxin exposure may be linked to the high prevalence of HIV in Southern Africa [7, 74, 118, 119]. The CD4 proteins that have been weakened by aflatoxin exposure have been reported to correlate positively with HIV infec‐ tion [116]. Also high aflatoxin levels have been reported to increase risk of developing tuber‐ culosis in HIV positive individuals. Persons who are exposed to aflatoxin and are HIV positive have decreased plasma vitamin A and vitamin E in the blood, although there was no interaction detected between aflatoxin and HIV infection [120]. HIV infection is likely to increase aflatoxin exposure by two possible routes: (1) HIV infection decreases the levels of antioxidant nutrients that promote the detoxification of aflatoxin, or (2) the high degree of co-infection of HIV-infected people with hepatitis B also increases the biological exposure to aflatoxin [7, 118, 119]. Aflatoxin induce immunosuppression and increases susceptibility of toxicated birds and animals to bacterial, viral and parasitic infections [58]. It also affects the lymphoid follicles of caecum thus depleting the lymphocytes that may contribute to the ob‐ served immunosuppression [117]. Aflatoxin decreases the concentrations of immunoglobu‐ lins IgM, IgG and IgA in birds as well as decrease complement activity in chickens [22, 121]. The low dose of AFB1 slightly decrease both mRNA and protein levels of lymphocytic IL-2, IFNγ and it preferentially affects macrophage functions as well as IL-1α, IL-6 and TNF pro‐ duction by these cells [121, 122]. Aflatoxin suppression of the immune system therefore sub‐ jects the individual to high risk of susceptible to infectious diseases like parasitic, bacterial and viral infections [123].

**References**

2(9), 254-263.

*mental Toxicology*, 55, 753-761.

ehc144.htm (Accessed on 19th June 2012) (1993).

boostjuice.com/AFLATOXICOSIS\_IN\_ANIMALS.pdf.

Base. *Toxnet (National Data Network)*.

culture\_and\_Trade/pdf, 10-15.

*NW Washington, DC 20006-1002 USA*, 1-16.

Feeds.pdf, 74.

497-516.

[1] Bankole, S. A., & Adebanjo, A. (2003). Review of mycotoxins in food in West Africa: current situation and possibilities of controlling it. *African Journal of Biotechnology*,

Review of the Biological and Health Effects of Aflatoxins on Body Organs and Body Systems

http://dx.doi.org/10.5772/51201

257

[2] Bennett, J. W., & Klich, M. (2003). Mycotoxins. *Clinical Microbiology Reviews*, 16(3),

[3] Gupta, R. C. (2011). Aflatoxins. *Ochratoxins and Citrinins. Reproductive and Develop‐*

[4] INCHEM Principles of evaluating chemical effects on the aged population: Interna‐ tional Programme on chemical Safety- Environmental Health Criteria 144 World Health Orgnization, Geneva,(1993). http://www.inchem.org/documents/ehc/ehc/

[5] Aflatoxins, N. L. M. (2002). National Library of Medicine. Hazardous Substance Data

[6] Thrasher, J. D. (2012). Aflatoxicosis in animals. *Aflatoxins and Health*, www.alpha‐

[7] USAID. (2012). Aflatoxin: A Synthesis of the Research in Health, Agriculture and Trade. *Feed the Future: The Office of Regional Economic Integration USAID East Africa Re‐ gional Mission Nairobi, Kenya*, www.eastafrica.usaid.gov/…esearch\_in\_Health\_Agri‐

[8] Whitlow, L.W.W., Hagler, M. J., & Diaz, D. E. (2010). mycotoxinsin in feeds. *Feed‐ stuffs*, http://fdsmagissues.feedstuffs.com/fds/Reference\_2010 13\_Mycotoxinsin‐

[9] WHO. (2000). Hazardous Chemicals in Humans and Environmental Health: Interna‐ tional Programme on Chemical safety, Geneva, Switzerland. *World Health Organisa‐*

[10] Wu, F., et al. (2011). *The Health economics of aflatoxins: Global burden of disease Aflacon‐ trol Working Paper 4 FebruaryInternational Food Policy Research Institute. 2033 K Street,*

[11] Lopez, C., et al. (2002). Aflatoxin B1 in human serum: Aflatoxin B1 content in pa‐

[12] Otsuki, T., Wilson, J. S., & Sewadeh, M. (2002). A Race to the Top? *A Case Study of Food Safety Standards and African Exports. Development Research Group (DECRG), World*

[13] Sudakin, D. L. (2003). Dietary aflatoxin exposure and chemoprevention of cancer: A

*Bank, 1818 H Street NW, Washington DC 20433 USA. 1424\_wps 2563.pdf*.

clinical review. *Journal of Toxicology and Clinical Toxicology*, 41, 195-204.

*tion*, http://whqlibdoc.who.int/hq/2000/WHO\_PCS\_00.1.pdf, 7-9.

tients with hepatic diseases. *Medicina (Buenos Aires)*, 313-316.
