Protective effects of l-arginine against testosterone synthesis decreased by T-2 toxin in mouse Leydig cells

Yang, Jian Ying; Zhang, Yong Fa; Nie, Na; Feng, Wen Po; Bao, Jianfeng; Meng, Xiang Ping; Xiao, Qiao

doi:10.1016/j.theriogenology.2019.05.023

Cited by 10 publications

(9 citation statements)

References 40 publications

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“…However, the process of detoxification is often accompanied by a loss of nutritional value of feeds and food crop by adding adsorbent to the contaminated products. Therefore, utilizing the addition of nutrients, such as L-arginine (Yang et al, 2019), L-carnitine (Moosavi et al, 2016), carotenoids (Leal et al, 1998), and N-acetyl-cysteine (He et al, 2012), to detoxify T-2 toxin was reported. L-Arginine, an -amino acid that is used in the biosynthesis of proteins (Bazer et al, 2015), is a precursor for the synthesis of many important metabolic molecules .…”

Section: Introductionmentioning

confidence: 99%

L-Arginine protects mouse Leydig cells against T-2 toxin-induced apoptosis in vitro

et al. 2020

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To explore the protective mechanism of L-arginine against T-2 toxin-induced apoptosis in mouse Leydig cells, we investigated whether L-arginine can prevent T-2 toxin-induced apoptosis in mouse Leydig cells and explored the underlying mechanisms. Leydig cells were isolated and cultured with control, T-2 toxin (10 nM), L-arginine (0.25, 0.5, and 1.0 mM), and T-2 toxin (10 nM T-2 toxin) + L-arginine (0.25, 0.5, or 1.0 mM) for 24 h. Cells and supernatants were harvested to examine proliferation of the cells, the apoptosis rate, activity of caspase-3 and mitochondria, and the gene expression levels of Bcl-2, Bax, PARP, and caspase-3. Results showed that proliferation and mitochondrial activity of Leydig cells were inhibited by administration of T-2 toxin. Bcl-2 gene expression levels was decreased, while the gene expression levels of Bax and PARP were increased, which could trigger mitochondria-mediated apoptosis, activate downstream caspase-3, and then increased caspase-3 at both activity and gene expression levels. The expression of the Bcl-2 gene was upregulated and the expression of Bax, caspase-3, and PARP gene were downregulated when L-arginine was added to the cultured cells. The results of this study showed that L-arginine could block T-2 toxin-induced apoptosis in mouse Leydig cells by regulating specific intracellular death-related pathways.

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Section: Introductionmentioning

confidence: 99%

L-Arginine protects mouse Leydig cells against T-2 toxin-induced apoptosis in vitro

et al. 2020

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“…Treatment with l -arginine increased the activities and mRNA expression of CAT, GSH-Px, and SOD and prevented DNA damage in primary mouse Leydig cells by defending against oxidative damage caused by T-2 toxin . Similarly, it was further revealed that l -arginine kept the T levels from being decreased by T-2 toxin by adjusting the mRNA expression levels and activities of StAR, P450scc, and 3β-HSD in mouse Leydig cells in vitro . Pretreatment with l -arginine supplementation in the mouse diets significantly improved semen quality, DSP, and the serum T content in mice exposed to T-2 toxin.…”

Section: Detoxification Of the Reproductive Toxicity Of T-2 Toxinmentioning

confidence: 83%

“…80 Similarly, it was further revealed that Larginine kept the T levels from being decreased by T-2 toxin by adjusting the mRNA expression levels and activities of StAR, P450scc, and 3β-HSD in mouse Leydig cells in vitro. 81 Pretreatment with L-arginine supplementation in the mouse diets significantly improved semen quality, DSP, and the serum T content in mice exposed to T-2 toxin. In addition, L-arginine can mitigate the decreased pregnancy rate and increased fetal resorption rate in females that are mated with male mice exposed to T-2 toxin.…”

Section: Detoxification Of the Reproductive Toxicity Of T-2 Toxinmentioning

confidence: 93%

Review of the Reproductive Toxicity of T-2 Toxin

Yang

Liu

Cui

et al. 2020

J. Agric. Food Chem.

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T-2 toxin, an inevitable environmental pollutant, is the most toxic type A trichothecene mycotoxin. Reproductive disruption is a key adverse effect of T-2 toxin. Herein, this paper reviews the reproductive toxicity of T-2 toxin and its mechanisms in male and female members of different species. The reproductive toxicity of T-2 toxin is evidenced by decreased fertility, disrupted structures and functions of reproductive organs, and loss of gametogenesis in males and females. T-2 toxin disrupts the reproductive endocrine axis and inhibits reproductive hormone synthesis. Furthermore, exposure to T-2 toxin during pregnancy results in embryotoxicity and the abnormal development of offspring. We also summarize the research progress in counteracting the reproductive toxicity of T-2 toxin. This review provides information toward a comprehensive understanding of the reproductive toxicity mechanisms of T-2 toxin.

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“…T-2 toxin triggers mice Leydig cell apoptosis. Furthermore, the toxin disrupts the hypothalamic–pituitary testicular axis, thus impairing the function of the testis and male fertility. ,, Despite some studies postulating that T-2 toxin affects male reproduction performance, the molecular mechanism involved in this damage is not completely known.…”

Section: Discussionmentioning

confidence: 99%

T-2 Toxin Caused Mice Testicular Inflammation Injury via ROS-Mediated NLRP3 Inflammasome Activation

Yang

Liu

Cui

et al. 2022

J. Agric. Food Chem.

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T-2 toxin treatment causes male reproduction system dysfunction, although the exact mechanism remains unclear. In this research, male Kunming mice and TM4 cells were treated with varying concentrations of the T-2 toxin for evaluating the adverse effect of T-2 toxin on male reproductive function. MCC950 or NAC was used to block NLRP3 inflammasome activation and eliminate reactive oxygen species (ROS) accumulation in the TM4 cell, respectively. The results showed that: (1) T-2 toxin caused testicular atrophy, destroyed the microstructure and ultrastructure of the testis, and caused sperm deformities; (2) T-2 toxin increased the content and gene expressions of TNF-α and IL-6 and decreased the IL-10 content and gene expression, causing testis and TM4 cell inflammatory injury; (3) T-2 toxin activated NLRP3 inflammasome in the testis and TM4 cells and caused ROS accumulation in the testis; (4) suppressing NLRP3 inflammasome activation using 20 nM MCC950 alleviated the TM4 cell inflammatory damage caused via the T-2 toxin; nevertheless, 20 nM MCC950 did not reduce ROS accumulation in TM4 cells; and (5) NAC relieved the inflammatory damage in TM4 cells by inhibiting NLRP3 inflammasome activation. Taken together, T-2 toxin caused testicular inflammation injury through ROS-mediated NLRP3 inflammasome activation, resulting in male reproductive dysfunction.

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Protective effects of l-arginine against testosterone synthesis decreased by T-2 toxin in mouse Leydig cells

Cited by 10 publications

References 40 publications

L-Arginine protects mouse Leydig cells against T-2 toxin-induced apoptosis in vitro

L-Arginine protects mouse Leydig cells against T-2 toxin-induced apoptosis in vitro

Review of the Reproductive Toxicity of T-2 Toxin

T-2 Toxin Caused Mice Testicular Inflammation Injury via ROS-Mediated NLRP3 Inflammasome Activation

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