T-2 toxin induced skin inflammation and cutaneous injury in mice

Agrawal, Mona; Yadav, Preeti; Lomash, Vinay; Bhaskar, A.S.B.; Rao, P. Venkata

doi:10.1016/j.tox.2012.08.007

Cited by 37 publications

(20 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T-2 is a type A trichothecene produced by several Fusarium species, mainly Fusarium sporotrichiodes, Fusarium poae and Fusarium langsethiae. Studies have demonstrated that T-2 affects the gastrointestinal tract, kidney, liver, heart, skin, the nervous, immunological, and reproductive systems, and embryogenic development in humans and animals (Agrawal et al, 2012;Li et al, 2011;Meissonnier et al, 2008).…”

Section: T-2 Toxinmentioning

confidence: 99%

“…Another apoptosis signalling pathway linked to oxidative stress induced by T-2 is through the activation of JNK1, p38 MAPK, increase in heat shock protein (Hsp) 70 expression, increase in iNOS activity and NO release, causing mitochondrial damage and activation of caspase 3 (Chaudhari and Lakshmana, 2010;Li and Pestka, 2008). In addition, studies have shown that T-2 can modulate the inflammatory response by increasing the expression of pro-inflammatory cytokines such as TNF-α, IL-6, IL-1β and IL-11 (Agrawal et al, 2012;Zhou et al, 2014).…”

Section: T-2 Toxinmentioning

confidence: 99%

See 1 more Smart Citation

Mycotoxins and oxidative stress: where are we?

Silva

Bracarense

Oswald

2018

WMJ

126

View full text Add to dashboard Cite

Mycotoxins are the most common contaminants of food and feed worldwide and are considered an important risk factor for human and animal health. Oxidative stress occurs in cells when the concentration of reactive oxygen species exceeds the cell’s antioxidant capacity. Oxidative stress causes DNA damage, enhances lipid peroxidation, protein damage and cell death. This review addresses the toxicity of the major mycotoxins, especially aflatoxin B1, deoxynivalenol, nivalenol, T-2 toxin, fumonisin B1, ochratoxin, patulin and zearalenone, in relation to oxidative stress. It summarises the data associated with oxidative stress as a plausible mechanism for mycotoxin-induced toxicity. Given the contamination caused by mycotoxins worldwide, the protective effects of a variety of natural compounds due to their antioxidant capacities have been evaluated. We review data on the ability of vitamins, flavonoids, crocin, curcumin, green tea, lycopene, phytic acid, L-carnitine, melatonin, minerals and mixtures of anti-oxidants to mitigate the toxic effect of mycotoxins associated with oxidative stress.

show abstract

Section: T-2 Toxinmentioning

confidence: 99%

Section: T-2 Toxinmentioning

confidence: 99%

Mycotoxins and oxidative stress: where are we?

Silva

Bracarense

Oswald

2018

WMJ

126

View full text Add to dashboard Cite

show abstract

“…Trichothecenes are also known to induce gene expression and release of proinflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) [1] , these cytokines can also contribute to anorexia induction by both peripheral and central administration [44] , [45] , [46] , [47] . T-2 toxin and SG were reported to cause mRNA levels of IL-1β, IL-6 and TNF-α upregulation in rodents [25] , [39] , [48] , [49] . It is therefore possible that anorexia induction by T-2 toxin, HT-2 toxin and SG might also be mediated in part by sickness responses to these cytokines.…”

Section: Discussionmentioning

confidence: 99%

Comparison of anorectic potencies of the trichothecenes T-2 toxin, HT-2 toxin and satratoxin G to the ipecac alkaloid emetine

Zhou

Pan

et al. 2015

Toxicology Reports

View full text Add to dashboard Cite

show abstract

“…Oxidative stress in liver and lipid peroxidation were shown to be related to suppression of phase I (cytochrome P450) and phase II (glutathione S‐ transferase) enzymes expression and activities in rats and rabbits fed with single or repeated oral dose of T‐2 toxin (Segal et al, ). Our earlier study has shown that topical application of T‐2 toxin resulted in skin oxidative stress in terms of increased reactive oxygen species generation, lipid peroxidation, and nuetrophil mediated myeloperoxidase activity (Agrawal et al, ).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of route of T-2 toxin exposure on hepatic oxidative damage in mice

2013

View full text Add to dashboard Cite

T-2 toxin is the most toxic among mycotoxins and poses a potential health hazard for both humans and animals. At high doses, T-2 toxin can cause shock-like syndrome that can result in death. We evaluated the effect of time course and route of exposure on hepatic oxidative damage in mice and it is only such study so far to compare the effects of dermal and subcutaneous exposure of T-2 toxin. Mice were exposed to 1 LD50 of T-2 toxin either by percutaneous (5.94 mg/kg body weight) or subcutaneous (1.54 mg/kg body weight) route and sacrificed at 0, 1, 3, and 7 days postexposure. Analysis of a number of serum biochemical variables, antioxidant enzymes activity, gene and protein expression by immunoblot assay showed time and route dependent effects of T-2 induced hepatic oxidative damage. Time dependent increase in protein carbonyl content and protein oxidation was seen in serum and liver. Results of our study may provide possible mechanism for developing medical countermeasures against T-2 toxin.

show abstract

T-2 toxin induced skin inflammation and cutaneous injury in mice

Cited by 37 publications

References 43 publications

Mycotoxins and oxidative stress: where are we?

Mycotoxins and oxidative stress: where are we?

Comparison of anorectic potencies of the trichothecenes T-2 toxin, HT-2 toxin and satratoxin G to the ipecac alkaloid emetine

Differential effects of route of T-2 toxin exposure on hepatic oxidative damage in mice

Contact Info

Product

Resources

About