Differential effects of T-2 toxin on bone marrow and spleen erythropoiesis in mice

Effects of multiple doses of T‐2 toxin on the erythroid response capacity of mice following an extensive experimental bleeding

“…However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996]. However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996].…”

“…Results from our laboratory clearly established that a single dose of T-2 toxin produces a strong but transient damage to iron-incorporating erythrocyte precursor cells [Faifer and Godoy, 1991], as well as granulocytic progenitor cells of mouse bone marrow, even at very small doses, while very little or no alterations were seen at the level of circulating blood [Faifer et al, 1992]. Further work using radiolabeled iron uptake into hematopoietic tissues confirmed that after single or several daily doses of T-2 toxin there was a strong damage to the erythropoietic precursor cells, which was rapidly reverted in spleen but not in bone marrow [Velazco et al, 1996]. According to the abundant literature on hematopoietic cytotoxicity, the extensive acute cytotoxic damage produced by T-2 toxin should be followed by a drastic recruitment of undifferentiated precursor cells [colony forming units-spleen cells (CFU-S)] TOXINS 5:152-156 (1997) into active proliferation [Goris et al, 1989;Hill, 1978].…”

Effects of multiple doses of T‐2 toxin on the erythroid response capacity of mice following an extensive experimental bleeding

“…However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996]. However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996].…”

“…Results from our laboratory clearly established that a single dose of T-2 toxin produces a strong but transient damage to iron-incorporating erythrocyte precursor cells [Faifer and Godoy, 1991], as well as granulocytic progenitor cells of mouse bone marrow, even at very small doses, while very little or no alterations were seen at the level of circulating blood [Faifer et al, 1992]. Further work using radiolabeled iron uptake into hematopoietic tissues confirmed that after single or several daily doses of T-2 toxin there was a strong damage to the erythropoietic precursor cells, which was rapidly reverted in spleen but not in bone marrow [Velazco et al, 1996]. According to the abundant literature on hematopoietic cytotoxicity, the extensive acute cytotoxic damage produced by T-2 toxin should be followed by a drastic recruitment of undifferentiated precursor cells [colony forming units-spleen cells (CFU-S)] TOXINS 5:152-156 (1997) into active proliferation [Goris et al, 1989;Hill, 1978].…”

Response of Channel Catfish to Diets Containing T-2 Toxin

“…Significant changes in cellularity were not reported in the spleen, but there were significant reductions in the number of B and T lymphocyte s among cells harvested from murine spleens (Smith et al 1994). The spleen of mice has been reported to rebound faster than bone marrow during continuous exposure to toxin, resulting in an initial hypoplasia followed by a compensatory hyperplasia, an adaptation not seen in bone marrow (Velazco et al 1996). A similar response in channel catfish could account for the lack of visible splenic cellular depletion when compared with that in the hematopoietic areas of the head kidney.…”

“…Functionally, chronic exposure to low levels of T-2 toxin produced immunosuppression in mice (both humoral and cell mediated [Corrier and Wagner 1988]), and mice showed increased susceptibility and lesion severity when challenged with Salmonella typhimurium (Tai and Pestka 1990). These experimental findings are reflected in the human disease alimentary toxic aleukia, which results from chronic T-2 toxin exposure and which is characterized by leukopenia, agranulocytosis, exhaustion of bone marrow, hemorrhage, and sepsis (Velazco et al 1996). Based on the histopathologic findings, it is reasonable to speculate that channel catfish that are chronically exposed to T-2 toxin would exhibit a lower number of circulating leukocytes and increased susceptibility to infectious diseases such as enteric septicemia of catfish (which is caused by the bacterium Edwardsiella ictaluri [Hawke 1979]).…”

T-2 Toxin, a Trichothecene Mycotoxin: Review of Toxicity, Metabolism, and Analytical Methods

“…Also, DNA ladders in bone marrow were clearly detected with agarose gel electrophoresis, indicating that the T-2 toxin-induced lesions in hematopoietic tissues and in lymphoid tissues were caused by apoptosis of component cells . Other studies revealed inhibition of DNA and protein synthesis in the spleen, thymus, and bone marrow after exposure to T-2, and T-2 had species-specific hemolytic effects on erythrocytes. , HL-60 human promyelocytic leukemia cells were used to characterize the apoptotic effects of T-2. Apoptotic cells were identified microscopically by chromatin condensation and nuclear fragmentation via flow cytometric analysis and DNA gel electrophorsis.…”

Effects of multiple doses of T‐2 toxin on the erythroid response capacity of mice following an extensive experimental bleeding

“…However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996]. However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996].…”

“…Results from our laboratory clearly established that a single dose of T-2 toxin produces a strong but transient damage to iron-incorporating erythrocyte precursor cells [Faifer and Godoy, 1991], as well as granulocytic progenitor cells of mouse bone marrow, even at very small doses, while very little or no alterations were seen at the level of circulating blood [Faifer et al, 1992]. Further work using radiolabeled iron uptake into hematopoietic tissues confirmed that after single or several daily doses of T-2 toxin there was a strong damage to the erythropoietic precursor cells, which was rapidly reverted in spleen but not in bone marrow [Velazco et al, 1996]. According to the abundant literature on hematopoietic cytotoxicity, the extensive acute cytotoxic damage produced by T-2 toxin should be followed by a drastic recruitment of undifferentiated precursor cells [colony forming units-spleen cells (CFU-S)] TOXINS 5:152-156 (1997) into active proliferation [Goris et al, 1989;Hill, 1978].…”

Response of Channel Catfish to Diets Containing T-2 Toxin

“…Significant changes in cellularity were not reported in the spleen, but there were significant reductions in the number of B and T lymphocyte s among cells harvested from murine spleens (Smith et al 1994). The spleen of mice has been reported to rebound faster than bone marrow during continuous exposure to toxin, resulting in an initial hypoplasia followed by a compensatory hyperplasia, an adaptation not seen in bone marrow (Velazco et al 1996). A similar response in channel catfish could account for the lack of visible splenic cellular depletion when compared with that in the hematopoietic areas of the head kidney.…”

“…Functionally, chronic exposure to low levels of T-2 toxin produced immunosuppression in mice (both humoral and cell mediated [Corrier and Wagner 1988]), and mice showed increased susceptibility and lesion severity when challenged with Salmonella typhimurium (Tai and Pestka 1990). These experimental findings are reflected in the human disease alimentary toxic aleukia, which results from chronic T-2 toxin exposure and which is characterized by leukopenia, agranulocytosis, exhaustion of bone marrow, hemorrhage, and sepsis (Velazco et al 1996). Based on the histopathologic findings, it is reasonable to speculate that channel catfish that are chronically exposed to T-2 toxin would exhibit a lower number of circulating leukocytes and increased susceptibility to infectious diseases such as enteric septicemia of catfish (which is caused by the bacterium Edwardsiella ictaluri [Hawke 1979]).…”

T-2 Toxin, a Trichothecene Mycotoxin: Review of Toxicity, Metabolism, and Analytical Methods

“…Also, DNA ladders in bone marrow were clearly detected with agarose gel electrophoresis, indicating that the T-2 toxin-induced lesions in hematopoietic tissues and in lymphoid tissues were caused by apoptosis of component cells . Other studies revealed inhibition of DNA and protein synthesis in the spleen, thymus, and bone marrow after exposure to T-2, and T-2 had species-specific hemolytic effects on erythrocytes. , HL-60 human promyelocytic leukemia cells were used to characterize the apoptotic effects of T-2. Apoptotic cells were identified microscopically by chromatin condensation and nuclear fragmentation via flow cytometric analysis and DNA gel electrophorsis.…”

Effects of multiple doses of T‐2 toxin on the erythroid response capacity of mice following an extensive experimental bleeding

“…However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996]. However, the multiple-dose regime provoked a more intense compensatory hypercellularity in spleen, which in this case lasted for about 20 days, instead of 4 days reported after a single dose [Velazco et al, 1996].…”

“…Results from our laboratory clearly established that a single dose of T-2 toxin produces a strong but transient damage to iron-incorporating erythrocyte precursor cells [Faifer and Godoy, 1991], as well as granulocytic progenitor cells of mouse bone marrow, even at very small doses, while very little or no alterations were seen at the level of circulating blood [Faifer et al, 1992]. Further work using radiolabeled iron uptake into hematopoietic tissues confirmed that after single or several daily doses of T-2 toxin there was a strong damage to the erythropoietic precursor cells, which was rapidly reverted in spleen but not in bone marrow [Velazco et al, 1996]. According to the abundant literature on hematopoietic cytotoxicity, the extensive acute cytotoxic damage produced by T-2 toxin should be followed by a drastic recruitment of undifferentiated precursor cells [colony forming units-spleen cells (CFU-S)] TOXINS 5:152-156 (1997) into active proliferation [Goris et al, 1989;Hill, 1978].…”

Response of Channel Catfish to Diets Containing T-2 Toxin

“…Significant changes in cellularity were not reported in the spleen, but there were significant reductions in the number of B and T lymphocyte s among cells harvested from murine spleens (Smith et al 1994). The spleen of mice has been reported to rebound faster than bone marrow during continuous exposure to toxin, resulting in an initial hypoplasia followed by a compensatory hyperplasia, an adaptation not seen in bone marrow (Velazco et al 1996). A similar response in channel catfish could account for the lack of visible splenic cellular depletion when compared with that in the hematopoietic areas of the head kidney.…”

“…Functionally, chronic exposure to low levels of T-2 toxin produced immunosuppression in mice (both humoral and cell mediated [Corrier and Wagner 1988]), and mice showed increased susceptibility and lesion severity when challenged with Salmonella typhimurium (Tai and Pestka 1990). These experimental findings are reflected in the human disease alimentary toxic aleukia, which results from chronic T-2 toxin exposure and which is characterized by leukopenia, agranulocytosis, exhaustion of bone marrow, hemorrhage, and sepsis (Velazco et al 1996). Based on the histopathologic findings, it is reasonable to speculate that channel catfish that are chronically exposed to T-2 toxin would exhibit a lower number of circulating leukocytes and increased susceptibility to infectious diseases such as enteric septicemia of catfish (which is caused by the bacterium Edwardsiella ictaluri [Hawke 1979]).…”

T-2 Toxin, a Trichothecene Mycotoxin: Review of Toxicity, Metabolism, and Analytical Methods

“…Also, DNA ladders in bone marrow were clearly detected with agarose gel electrophoresis, indicating that the T-2 toxin-induced lesions in hematopoietic tissues and in lymphoid tissues were caused by apoptosis of component cells . Other studies revealed inhibition of DNA and protein synthesis in the spleen, thymus, and bone marrow after exposure to T-2, and T-2 had species-specific hemolytic effects on erythrocytes. , HL-60 human promyelocytic leukemia cells were used to characterize the apoptotic effects of T-2. Apoptotic cells were identified microscopically by chromatin condensation and nuclear fragmentation via flow cytometric analysis and DNA gel electrophorsis.…”