Effect of T-2 toxin-injected shrimp muscle extracts on mouse macrophage cells (RAW264.7)

Huang, Zhanrui; Wang, Yaling; Qiu, Mei; Sun, Lijun; Liao, Jianmeng; Wang, Rundong; Sun, Xiaodong; Bi, Siyuan; Gooneratne, Ravi

doi:10.1080/01480545.2016.1278227

Cited by 12 publications

(6 citation statements)

References 21 publications

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“…A wealth of research papers clearly indicate a negative influence of T-2 toxin on the hematocytes, hepatocytes, chondrocytes, intestinal function, immune system, and reproductive system (Adhikari et al, 2017; He et al, 2012; Huang et al, 2018; Leal et al, 1998; Moosavi et al, 2016; Wu et al, 2017; Yang et al, 2010; Zhang et al, 2018). Our research team has also reported the negative effects of T-2 toxin on male fertility and other reproductive pathologies in male animals (Yang et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Delayed effects of autophagy on T-2 toxin-induced apoptosis in mouse primary Leydig cells

et al. 2019

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T-2 toxin is a type-A trichothecene produced by Fusarium found in several food commodities worldwide. T-2 toxin causes reproductive disorders, genotoxicity, and testicular toxicity in animals. Our previous research has reported that T-2 toxin can induce apoptosis via the Bax-dependent caspase-3 activation in mouse primary Leydig cells. However, little is known about the functions of autophagy and the cross talk between autophagy and apoptosis after exposure to T-2 toxin in Leydig cells. This study investigated these problems in mouse primary Leydig cells. Results showed that T-2 toxin treatment upregulated LC3-II and Beclin-1 expression, suggesting that T-2 toxin induced a high level of autophagy. Pretreatment with chloroquine (an autophagy inhibitor) and rapamycin (an autophagy inducer) increased and decreased the rate of apoptosis, respectively, in contrast to T-2 toxin-treated group. Autophagy delayed apoptosis in the T-2 toxin-treated Leydig cells. Therefore, autophagy may prevent cells from undergoing apoptosis by reducing T-2 toxininduced cytotoxicity.

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Section: Discussionmentioning

confidence: 99%

Delayed effects of autophagy on T-2 toxin-induced apoptosis in mouse primary Leydig cells

et al. 2019

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“…Contamination of feed ingredients with toxic concentrations of mycotoxins has been so serious in recent years, that it seems likely to limit the expansion of aquaculture in Asia 28,29 . It has been shown that dietary aflatoxin B 1 caused poor growth performance and deformities of juvenile grass carp 30 .…”

Section: Discussionmentioning

confidence: 99%

Effects of T-2 toxin on digestive enzyme activity, intestinal histopathology and growth in shrimp Litopenaeus vannamei

Huang

Wang

Qiu

et al. 2019

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T-2 toxin (T-2), a naturally occurring mycotoxin that often accumulates in aquatic animals via contaminated feed, is toxic to animals, including humans. In this study, six groups of shrimp (n = 30 shrimps/group) were given T-2 in feed at concentrations of 0–12.2 mg/kg for 20 days. T-2 accumulation, intestinal histopathology, digestive enzyme activities and subsequent effects on shrimp are reported. Compared to the control, T-2 significantly reduced weight gain, specific growth rate, and survival. The histopathology of shrimp intestine showed concentration-dependent degenerative and necrotic changes in response to dietary T-2. Progressive damage to the microstructures of shrimp intestine occurred with increasing dietary T-2 concentrations, with initial inflammation of the mucosal tissue at T-2 concentrations of 0.5 and 1.2 mg/kg, progressing to disappearance of intestinal villi and degeneration and necrosis of the submucosa at 12.2 mg/kg. Intestinal amylase and protease activities increased at low T-2 concentrations but showed significant inhibition at high concentrations; however, the opposite trend occurred for lipase activity. Collectively, these results indicate that digestive enzyme activities and mucosal structures are markedly affected by exposure to T-2, and these may have contributed to the lower survival rate of shrimp.

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“…T-2 toxin, a fungal secondary metabolite, has immunotoxic, hepatotoxic, hematotoxic, and genotoxic properties (Adhikari et al, 2017; Huang et al, 2018; Wu et al, 2017; Yang et al, 2010; Zhang et al, 2018). T-2 toxin has been shown to induce apoptosis in lymphocytes (Shinozuka et al, 1997), thymocytes (Islam et al, 1998), rat ovarian granulosa cells (Wu et al, 2013), human chondrocytes (Liu et al, 2014), human neuroblastoma cells (Agrawal et al, 2015), and mouse Leydig cells (Zhang et al, 2018).…”

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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Effect of T-2 toxin-injected shrimp muscle extracts on mouse macrophage cells (RAW264.7)

Cited by 12 publications

References 21 publications

Delayed effects of autophagy on T-2 toxin-induced apoptosis in mouse primary Leydig cells

Delayed effects of autophagy on T-2 toxin-induced apoptosis in mouse primary Leydig cells

Effects of T-2 toxin on digestive enzyme activity, intestinal histopathology and growth in shrimp Litopenaeus vannamei

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

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