Determination of the Acute 50% Lethal Dose T-2 Toxin in Adult Bobwhite Quail: Additional Studies on the Effect of T-2 Mycotoxin on Blood Chemistry and the Morphology of Internal Organs

Abstract

Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.

Oxidative stress induction by T-2 toxin causes DNA damage and triggers apoptosis via caspase pathway in human cervical cancer cells

“…In vitro T-2 toxin causes apoptosis in various cell types like HL60, Jurkat, U937 (Huang et al, 2007), Vero cells (Bouaziz et al, 2006) and human hepatoma cells (Bouaziz et al, 2008). Apoptosis was also reported in vivo in thymic and spleenic lymphocytes as well as other tissues of mice like bone marrow and intestinal epithelial cells (Li et al, 1997;Shinozuka et al, 1997), skin (Albarenque et al, 1999), kidney (Grizzle et al, 2004) and brain (Sehata et al, 2004).…”

The effect of T-2 toxin on percentages of CD4+, CD8+, CD4+CD8+ and CD21+ lymphocytes, and mRNA expression levels of selected cytokines in porcine ileal Peyer’s patches

“…Due to its hematotoxic effects, it impairs the immune response. The exposure to the T-2 toxin causes leukopenia and cell depletion in lymphoid organs, it inhibits erythropoiesis in the bone marrow and spleen (Nagata et al 2001, Grizzle et al 2004, Parent-Massin 2004. T-2 intoxication can significantly impair antibody production (Niyo et al 1988, Kamalavenkatesh et al 2005, Li et al 2006a, it reduces the proliferative response of lymphocytes (Rafai et al 1995, Kamalavenkatesh et al 2005 and hinders the development of dendritic cells (Hymery et al 2006, Hymery et al 2009).…”

Subclinical doses of T-2 toxin impair acquired immune response and liver cytochrome P450 in pigs

“…In addition T-2 toxin impairs the immune response, principally due to its hematotoxic properties. Exposure to this mycotoxin induces leucopenia and cell depletion in lymphoid organs, and inhibition of erythropoiesis in bone marrow and spleen (Nagata et al, 2001;Grizzle et al, 2004;Parent-Massin, 2004). The production of antibodies can also be impaired (Niyo et al, 1988;Kamalavenkatesh et al, 2005;Li et al, 2006a,b).…”