Role of nutrition in the survival after hepatotoxic injury

Hepatocyte Ploidy in Regenerating Livers after Partial Hepatectomy, Drug-Induced Necrosis, and Cirrhosis

“…We found that this was associated with a marked decrease in the number of viable hepatocytes isolated from those livers, as also observed by Diez-Fernandez et al [52] in TA-treated rats. As previously described by Chanda and Mehendale [56] and Theocharis et al [57] after sublethal TA injection, we found a return to basal aminotransferase values 7-12 days after sublethal injection of both TA and GalN.…”

Hepatocyte Ploidy in Regenerating Livers after Partial Hepatectomy, Drug-Induced Necrosis, and Cirrhosis

“…We found that this was associated with a marked decrease in the number of viable hepatocytes isolated from those livers, as also observed by Diez-Fernandez et al [52] in TA-treated rats. As previously described by Chanda and Mehendale [56] and Theocharis et al [57] after sublethal TA injection, we found a return to basal aminotransferase values 7-12 days after sublethal injection of both TA and GalN.…”

Role of tissue repair in toxicologic interactions among hepatotoxic organics.

“…However, the previous two examples illustrate that the sole use of differences in bioactivation mechanisms as the basis for interspecies extrapolation cannot be justified. (37,66). In addition to thioacetamide, glucose loading also increased the mortality of CC14, CHCl3, and acetaminophen, suggesting that this effect is not related to chemical structure or mechanism of infliction of injury (37,67 (68).…”

Functional Relationships between Lipid Metabolism and Liver Regeneration

“…Extending this paradigm, other studies show that either intravenous or enteral dextrose supplementation suppresses both PH- [18–24] and toxin- (CCl 4 , thioacetamide; [25, 26] and J. Huang and D.A. Rudnick, unpublished observations) -induced hepatocellular proliferation.…”

Hepatocyte Ploidy in Regenerating Livers after Partial Hepatectomy, Drug-Induced Necrosis, and Cirrhosis

“…We found that this was associated with a marked decrease in the number of viable hepatocytes isolated from those livers, as also observed by Diez-Fernandez et al [52] in TA-treated rats. As previously described by Chanda and Mehendale [56] and Theocharis et al [57] after sublethal TA injection, we found a return to basal aminotransferase values 7-12 days after sublethal injection of both TA and GalN.…”

Role of tissue repair in toxicologic interactions among hepatotoxic organics.

“…However, the previous two examples illustrate that the sole use of differences in bioactivation mechanisms as the basis for interspecies extrapolation cannot be justified. (37,66). In addition to thioacetamide, glucose loading also increased the mortality of CC14, CHCl3, and acetaminophen, suggesting that this effect is not related to chemical structure or mechanism of infliction of injury (37,67 (68).…”

Functional Relationships between Lipid Metabolism and Liver Regeneration

“…Extending this paradigm, other studies show that either intravenous or enteral dextrose supplementation suppresses both PH- [18–24] and toxin- (CCl 4 , thioacetamide; [25, 26] and J. Huang and D.A. Rudnick, unpublished observations) -induced hepatocellular proliferation.…”

Hepatocyte Ploidy in Regenerating Livers after Partial Hepatectomy, Drug-Induced Necrosis, and Cirrhosis

“…We found that this was associated with a marked decrease in the number of viable hepatocytes isolated from those livers, as also observed by Diez-Fernandez et al [52] in TA-treated rats. As previously described by Chanda and Mehendale [56] and Theocharis et al [57] after sublethal TA injection, we found a return to basal aminotransferase values 7-12 days after sublethal injection of both TA and GalN.…”

Role of tissue repair in toxicologic interactions among hepatotoxic organics.

“…However, the previous two examples illustrate that the sole use of differences in bioactivation mechanisms as the basis for interspecies extrapolation cannot be justified. (37,66). In addition to thioacetamide, glucose loading also increased the mortality of CC14, CHCl3, and acetaminophen, suggesting that this effect is not related to chemical structure or mechanism of infliction of injury (37,67 (68).…”

Functional Relationships between Lipid Metabolism and Liver Regeneration

“…Extending this paradigm, other studies show that either intravenous or enteral dextrose supplementation suppresses both PH- [18–24] and toxin- (CCl 4 , thioacetamide; [25, 26] and J. Huang and D.A. Rudnick, unpublished observations) -induced hepatocellular proliferation.…”