Spermatogenesis disorder caused by T-2 toxin is associated with germ cell apoptosis mediated by oxidative stress

Yang, Xu; Zhang, Xuliang; Zhang, Jian; Ji, Qiang; Huang, Wanyue; Zhang, Xueyan; Li, Yanfei

doi:10.1016/j.envpol.2019.05.023

Cited by 72 publications

(27 citation statements)

References 41 publications

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“…Oxidative stress can also be assessed by detecting the testis content of MDA and GSH, as well as the activities of T-AOC, CAT, and SOD. In our study, we found that T-2 toxin significantly reduced the activity of T-AOC, CAT, and SOD, and reduced the content of GSH while it increased the content of MDA; these data are consistent with previous research results [32]. In line with this, the present study showed that T-2 toxin also caused testicular damage in mice, decreased the number of mesenchymal cells, and reduced serum testosterone levels and sperm motility, which was consistent with previous studies [32].…”

Section: Discussionsupporting

confidence: 93%

“…There is evidence suggesting that T-2 toxin could induce germ cell apoptosis by regulating the expression of Bcl-2 family and caspase family apoptosis-related genes in the mitochondrial signaling pathway. The expression of caspase-8 mRNA was increased, suggesting that the apoptosis of germ cells may be related to the death receptor pathway [32]. The Bcl-2 gene family regulates apoptosis through the mitochondrial pathway.…”

Section: Discussionmentioning

confidence: 99%

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Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

Yang

Liu

et al. 2019

Biomolecules

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T-2 toxin is one of the most toxic type A trichothecene mycotoxins in nature, and it exhibits reproductive toxicity. Betulinic acid (BA) is a natural pentacyclic triterpene compound found in species of Betula, and it has been reported to have antioxidant activity. The aim of the present study was to investigate the protective effect of BA on T-2-toxin-induced testicular injury in mice and explore its molecular mechanism. Sixty adult male mice were randomly divided into groups. The mice were pretreated orally with BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and the T-2 toxin (4 mg/kg body weight) was administered via intraperitoneal injection to induce oxidative stress after the last administration of BA. BA pretreatment significantly increased the secreted levels of testosterone and sperm motility. Moreover, BA pretreatment significantly increased the total antioxidant capacity (T-AOC), the activity of SOD and CAT, and the content of GSH, and it reduced the content of MDA. Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax). BA also increased the expression of B-cell lymphoma-2 (Bcl-2). We suggest that BA reduced the oxidative damage induced by T-2 toxin, and that these protective effects may be partially mediated by the JAK2/STAT3 signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

Yang

Liu

et al. 2019

Biomolecules

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“…The decrease in maternal nutritional levels may reduce the birth weight of the offspring, thereby reduce its production performance [21]. In the present study, a significant decrease in body weight and testicular weight was detected in the maternal exposure of T-2 toxin group, and these results were consistent with previous findings of the direct effects of T-2 toxin on mice [16]. The inhibition of the seminiferous tubules' development (PND 21 histological section) and the increase of the seminiferous tubule gaps (PND 28) may be the cause of testicular weight loss in offspring.…”

Section: Maternal Exposure To T-2 Toxin Induced Decreases In Body Weisupporting

confidence: 93%

“…T-2 toxin has been shown to decrease the activity of antioxidant enzymes such as SOD, GSH-Px, and CAT mainly via oxidative stress [30]. The latest studies showed that increased oxidative damage was detected in oral T-2 toxin treated mice, with the increase in ROS and MDA and decrease in T-AOC and GSH-Px, accompanied by disordered spermatogenesis [16]. In the present study, maternal exposure to T-2 toxin reduced the activity of SOD and increased the level of MDA in the testes in pre-puberty; moreover, a significant decrease in testicular testosterone was detected in pre-puberty.…”

Section: Maternal Exposure To T-2 Toxin Induced Oxidative Stress In Tmentioning

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%

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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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Arsenic and polystyrene‐nano plastics co‐exposure induced testicular toxicity: Triggers oxidative stress and promotes apoptosis and inflammation in mice

Rao,

Qiao,

Zhong

et al. 2023

Environmental Toxicology

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Co‐existing of polystyrene‐nano plastics (PSNPs) and arsenic (As) in the environment caused a horrendous risk to human health. However, the potential mechanism of PSNPs and As combination induced testicular toxicity in mammals has not been elucidated. Therefore, we first explore the testicular toxicity and the potential mechanism in male Kunming mice exposed to As or/and PSNPs. Results revealed that compared to the As or PSNPs group, the combined group showed more significant testicular toxicity. Specifically, As and PSNPs combination induced irregular spermatozoa array and blood–testis barrier disruption. Simultaneously, As and PSNPs co‐exposure also exacerbated oxidative stress, including increasing the MDA content, and down‐regulating expression of Nrf‐2, HO‐1, SOD‐1, and Trx. PSNPs and As combination also triggered testicular apoptosis, containing changes in apoptotic factors (P53, Bax, Bcl‐2, Cytc, Caspase‐8, Caspase‐9, and Caspase‐3). Furthermore, co‐exposed to As and PSNPs aggravated inflammatory damage characterized by targeted phosphorylation of NF‐κB and degradation of I‐κB. In summary, our results strongly confirmed As + PSNPs co‐exposure induced the synergistic toxicity of testis through excessive oxidative stress, apoptosis, and inflammation, which could offer a new sight into the mechanism of environmental pollutants co‐exposure induced male reproductive toxicity.

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Spermatogenesis disorder caused by T-2 toxin is associated with germ cell apoptosis mediated by oxidative stress

Cited by 72 publications

References 41 publications

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

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

Arsenic and polystyrene‐nano plastics co‐exposure induced testicular toxicity: Triggers oxidative stress and promotes apoptosis and inflammation in mice

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