“
“Acrolein is a toxic unsaturated aldehyde and widespread environmental pollutant produced during lipid peroxidation and also by burning of tobacco or
liquid fuels. Inhalation or dermal exposure to acrolein could be toxic to organisms. This very reactive aldehyde has a strong affinity for binding to proteins thus forming pathogenic protein-adducts. In the present study we have analyzed formation of bioreactive acrolein-protein adducts in bovine serum albumin solution exposed to exhaust gases of mineral diesel fuel and of mineral diesel fuel supplemented with different amounts of a novel diesel fuel additive denoted Ecodiesel (produced by a genuine procedure of recycling of plant oils used for food preparation). The effects of acrolein-protein adducts were tested on human microvascular endothelial cells and on human osteosarcoma cells that are sensitive to bioactivities of lipid peroxidation this website products. The results have shown a reduction of the bioreactive acrolein in exhaust gases when mineral diesel was supplemented with 520% Ecodiesel. Moreover, acrolein-protein adducts obtained from mineral diesel supplemented with Ecodiesel were less toxic than those obtained
from mineral diesel alone. Thus, we assume that supplementing mineral diesel fuel with Ecodiesel would be of benefit for the use of renewable energy, for environment and for human health due to reduced environmental pollution with bioreactive acrolein. (c) 2011 Wiley Periodicals, MAPK inhibitor Inc. Environ Toxicol, 2011.”
“J. Michael Wentzell, MD, has indicated no significant interest with commercial supporters.”
“The 3-methyl-4-nitrophenol (4-nitro-m-cresol; PNMC) exists in diesel exhaust particles (DEP), and is also one of the degradation products of insecticide fenitrothion. To assess potential nephrotoxicity of PNMC, male Sprague-Dawley (SD) rats were subcutaneously dosed with PNMC at 1, 10, and 100 mg/kg/day for five consecutive days. No significant changes were detected in body
weights and relative BMS345541 weights of kidneys by the treatment of PNMC. However, the extent of cellular necrosis was found to be severe in renal tubular epithelial cells of PNMC-treated rats. In addition, PNMC exposure significantly increased the number of terminal deoxynucleotidyle transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells compared to the control in renal tubule of PNMC-treated rats. Moreover, immunohistochemical results indicated that significant decrease in the B-cell lymphoma 2 (Bcl-2) expressions andincrease in the Bcl-2 associated x protein (Bax) expression were detected in PNMC-treated rats. The ratio of Bcl-2/Bax was also reduced significantly at PNMC-treated rats dosed at 10 or 100 mg kg-1. Furthermore, the significant increase of FAS (CD95/APO-1) expression was found in the groups dosed at 10 or 100 mg kg-1 of PNMC. The expression of Caspase-3 was higher in PNMC-treated rats, compared to the control group.