T-2 toxin impairs male fertility by disrupting hypothalamic-pituitary-testis axis and declining testicular function in mice

Yang, Xu; Zhang, Xuliang; Yao, Qiucheng; Song, Miao; Han, Yaling; Lei, Lei; Li, Yanfei

doi:10.1016/j.chemosphere.2019.06.145

Cited by 44 publications

(29 citation statements)

References 44 publications

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“…Symptoms of acute poisoning include vomiting, hemorrhagic dysfunction, and cardiovascular dysfunction (such as endotoxin shock) [ 6 ], while chronic poisoning symptoms include loss of appetite, weight loss, and oral and esophageal lesions, among others [ 7 ]. According to some studies, T-2 toxin has many toxic effects, include immunotoxicity [ 8 ], reproductive toxicity [ 9 ], hematotoxicity [ 10 ], hepatotoxicity [ 2 ], neurotoxicity [ 11 ], cardiotoxicity [ 12 ], and bone system damage [ 13 ] ( Table 1 ).…”

Section: Introductionmentioning

confidence: 99%

Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway

Zhu

et al. 2020

Toxins

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T-2 toxin, the most toxic of the trichothecenes, is widely found in grains and feeds, and its intake poses serious risks to the health of humans and animals. An important cytotoxicity mechanism of T-2 toxin is the production of excess free radicals, which in turn leads to oxidative stress. Betulinic acid (BA) has many biological activities, including antioxidant activity, which is a plant-derived pentacyclic triterpenoid. The protective effects and mechanisms of BA in blocking oxidative stress caused by acute exposure to T-2 toxin in the thymus of mice was studied. BA pretreatment reduced ROS production, decreased the MDA content, and increased the content of IgG in serum and the levels of SOD and GSH in the thymus. BA pretreatment also reduced the degree of congestion observed in histopathological tissue sections of the thymus induced by T-2 toxin. Besides, BA downregulated the phosphorylation of the p38, JNK, and ERK proteins, while it upregulated the expression of the Nrf2 and HO-1 proteins in thymus tissues. The results indicated that BA could protect the thymus against the oxidative damage challenged by T-2 toxin by activating Nrf2 and suppressing the MAPK signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway

Zhu

et al. 2020

Toxins

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“…Insufficient testosterone secretion at any period will affect the normal development of the testes. In previous studies, direct exposure of T-2 toxin could inhibit the mRNA expression of 3β-HSD, CYP11A1 and StAR in mouse Leydig cells [38] and impaired testosterone secretion in vitro [39,40] and vivo [17] model. The data detected in the present study showed that after the maternal exposure of T-2 toxin, the genes involved in testosterone synthesis were down-regulated in the testes of pre-puberty offspring, especially StAR, the essential limiting factor in testosterone synthesis.…”

Section: Maternal Exposure Of T-2 Toxin Inhibited Testosterone Synthementioning

confidence: 99%

“…Reproductive dysfunction was the major detrimental effect of T-2 toxin [15]. In recent years, the research of T-2 toxin on the reproductive system has gradually increased and the effects of direct exposure to T-2 toxin on reproduction have been reported in several studies [16,17]. It is of great practical significance to reveal the toxicity mechanism of T-2 toxin on the male reproductive system.…”

Section: Introductionmentioning

confidence: 99%

Maternal Exposure to T-2 Toxin Induces Changes in Antioxidant System and Testosterone Synthesis in the Testes of Mice Offspring

Shen

Perveen

Kaka

et al. 2019

Animals

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T-2 toxin, the most toxic member of trichothecene mycotoxin, is widely distributed in cereals, and has been extensively studied, but few studies focus on the toxicity of maternal exposure to offspring. This study focused on the effects of maternal exposure to T-2 toxin (during gestation and lactation) on the testicular development of mice offspring. Dams were orally administered with T-2 toxin at 0, 0.005, or 0.05 mg/kg body weight from the late stage of gestation to the end of lactation. Testicular samples of the mice offspring were collected on the postnatal day 21, 28, and 56. The results showed significant decreases in body weight and testicular weight on the postnatal day 28. Moreover, significant inhibition of antioxidant system and testosterone synthesis was detected on the postnatal day 28. Furthermore, there were significant decreases in the gene expression levels of StAR and 3β-HSD, which are involved in testosterone synthesis. In general, present results demonstrated that maternal exposure to T-2 toxin during gestation and lactation led to bad effects on the capacity of antioxidant system and inhibited testosterone synthesis in testes during pre-puberty with no significant effects on post-puberty.

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“…T-2 toxin is readily absorbed by the gastrointestinal tract, exerts a wide range of toxic effects on multiple tissues and organs including the liver, kidney, spleen, testis and bone. [2][3][4][5][6] Studies have shown that the content of T-2 toxin in skeletal system is higher than that in other tissues and organs, especially in the femur. 7 Several epidemiological investigations have suggested that T-2 toxin is the major risk factor for Kashin-Beck disease (KBD) in China.…”

Section: Introductionmentioning

confidence: 99%

T‐2 toxin‐induced femur lesion is accompanied by autophagy and apoptosis associated with Wnt/β‐catenin signaling in mice

Zhang

Song

Cui

et al. 2022

Environmental Toxicology

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T-2 toxin is one of the most common mycotoxins found in grain foods, animal feed, and other agricultural by-products causing food contamination and health threat. The skeletal system is the main target tissue for T-2 toxin. T-2 toxin exposure is also recognized as a potential contributor to multiple types of bone diseases, including Kashin-Beck disease. However, the mechanisms of T-2 toxin-induced bone toxicity remain unclear. In this study, 60 male C57BL/6 mice were exposed T-2 toxin with 0, 0.5, 1 or 2 mg/kg body weight by intragastric administration for 28 days, respectively. Femora were collected for the detections of femur lesion, bone formation factors, oxidative stress, autophagy, apoptosis, and Wnt/β-catenin signaling. Our research showed that T-2 toxin caused bone formation disorders, presenting as the reduction of the BMD and femur length, bone structure changes and abnormal bone formation proteins expressions, along with enhanced oxidative stress. Meanwhile, T-2 toxin increased expressions of autophagy-related proteins (Beclin 1, ATG5, p62, and LC3), and promoted apoptosis in mouse femur. Moreover, T-2 toxin suppressed the Wnt/β-catenin signaling and expressions of downstream target genes. Taken together, our data indicated T-2 toxin-induced femur lesion was accompanied by autophagy and apoptosis, which was associated with Wnt/β-catenin signaling.

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T-2 toxin impairs male fertility by disrupting hypothalamic-pituitary-testis axis and declining testicular function in mice

Cited by 44 publications

References 44 publications

Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway

Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway

Maternal Exposure to T-2 Toxin Induces Changes in Antioxidant System and Testosterone Synthesis in the Testes of Mice Offspring

T‐2 toxin‐induced femur lesion is accompanied by autophagy and apoptosis associated with Wnt/β‐catenin signaling in mice

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