Effect of Aflatoxin B1 on Histopathology and Oxidative Stress Biomarkers in Testis of Rats with Special References to Gene Expression of Antioxidant Enzymes

Althnaian, Thnaian A.; Albokhadai, I.F.; El-Bahr, Sabry M.

doi:10.3923/ijp.2016.408.414

Cited by 7 publications

(2 citation statements)

References 15 publications

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“…Another possibility would be the ability of AFB1 to bind to the acute steroidogenic regulatory protein (STAR), thus affecting the transfer of cholesterol to the mitochondria, which has a negative impact on steroidogenesis [ 30 ]. Direct cellular damage caused by oxidative stress should also be considered, as already evidenced by Althnaian et al [ 33 ], who found substantial increases in oxidative stress markers and decreases in antioxidant enzymes in the testicles of rats exposed to a single intraperitoneal application of 3 mg/kg of AFB1 [ 33 ]. AFB1 also affects the reproductive capacity of females, although in lower intensity, causing follicular atresia [ 32 ].…”

Section: Effects Of Prenatal Exposure To Aflatoxin B1 In Animalsmentioning

confidence: 99%

Effects of Prenatal Exposure to Aflatoxin B1: A Review

2021

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Aflatoxins are mycotoxins produced as secondary fungal metabolites. Among them, aflatoxin B1 (AFB1) stands out due to its genotoxic and mutagenic potential, being a potent initiator of carcinogenesis. In this review, the outcomes from the published literature in the past 10 years on the effects of AFB1 pathophysiological mechanisms on embryological and fetal development are discussed. In several animal species, including humans, AFB1 has a teratogenic effect, resulting in bone malformations, visceral anomalies, lesions in several organs, and behavioral and reproductive changes, in addition to low birth weight. The mutagenic capacity of AFB1 in prenatal life is greater than in adults, indicating that when exposure occurs in the womb, the risk of the development of neoplasms is higher. Studies conducted in humans indicate that the exposure to this mycotoxin during pregnancy is associated with low birth weight, decreased head circumference, and DNA hypermethylation. However, as the actual impacts on humans are still unclear, the importance of this issue cannot be overemphasized and studies on the matter are essential.

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Section: Effects Of Prenatal Exposure To Aflatoxin B1 In Animalsmentioning

confidence: 99%

Effects of Prenatal Exposure to Aflatoxin B1: A Review

2021

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“…Any structural changes including histomorphometric and spermiogenic alterations could be related to the toxic agent‐induced direct and/or indirect actions. We and others previously showed that not only CPA exposure but other mycotoxins including aflatoxin B1, ochratoxin A, fumonesin B1, and zearalenone exposure resulted in direct structural changes such as vacuolation in spermatogonia, creation of multinuclear giant cells, disorganization, changes in the number and thickness of spermatogenesis cell series, atrophy and necrosis of the seminiferous tubules, thickening in the basement membrane of the testis and epithelium of the seminiferous tubules 50‐55 . The direct effects of toxicants may related to their chemical reactivity with target site and/or any changes in the function of various cells and organelles.…”

Section: Discussionmentioning

confidence: 95%

Cyclopiazonic acid induced p53‐dependent apoptosis in the testis of mice: Another male related risk factor of infertility

Bonyadi

Hasanzadeh

Malekinejad

2021

Environmental Toxicology

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Cyclopiazonic acid (CPA) is an indole tetrameric acid mycotoxin. This study carried out to investigate the potential effects of CPA on male reproductive system. In the current study, 40 adult male mice were divided into five groups (n = 8). The control group did not expose to CPA, while animals in vehicle‐received group; received the CPA‐solvent (0.05% dimethyl sulfoxide) and the animals of third, fourth, and fifth groups received CPA 0.03, 0.06, and 0.12 mg/kg, body weight, respectively for 28 days. Morphometric and morphological deviations, spermatogenesis indices, malondialdehyde (MDA) content, total thiol molecules (TTM) concentration, total antioxidant capacity (TAC), protein carbonylation rate (CO), and nitric oxide (NO) concentration were examined. The expression changes of apoptotic genes (P53, Bcl‐2, and Caspase III) at mRNA level were also evaluated by qPCR technique. Reduction in the Leydig and Sertoli cells population, diameter of seminiferous tubules, and spermatogenesis parameters was significant only in the group that received the highest dose of CPA. An increase in the level of MDA, NO, and CO in testicular tissue and reduction of TAC and TTM were observed in the CPA‐exposed groups. Significant up‐regulation (p < .05) in the expression of P53 and Caspase III genes and down‐regulation of Bcl‐2 gene were found in the CPA‐received groups. These results are indicating the detrimental effects of CPA on the testicles, which may attribute to the CPA‐induced oxidative stress and apoptosis. Moreover, results also help to understand a serious concern about the presence of CPA in foods as a potential risk factor in male‐related infertility.

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Oxidative DNA damage and multi-organ pathologies in male mice subchronically treated with aflatoxin B1

Zhou

Wang²,

et al. 2019

Ecotoxicology and Environmental Safety

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Effect of Aflatoxin B1 on Histopathology and Oxidative Stress Biomarkers in Testis of Rats with Special References to Gene Expression of Antioxidant Enzymes

Cited by 7 publications

References 15 publications

Effects of Prenatal Exposure to Aflatoxin B1: A Review

Effects of Prenatal Exposure to Aflatoxin B1: A Review

Cyclopiazonic acid induced p53‐dependent apoptosis in the testis of mice: Another male related risk factor of infertility

Oxidative DNA damage and multi-organ pathologies in male mice subchronically treated with aflatoxin B1

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