PHARM.D

                      yellow phosphorous poisoning yellow phosphorous was once used as a rat or roach poison . Fire works and fertilizers manufactures which release phosphine on contact with water. DOSE: The fatal dose of yellow phosphorous or phosphite is approximatyely 1mg/kg. The exposure limit for yellow phosphorous is 0.1 mg/m3; for phosphine , 0.3 ppm;and for phenyl phosphine,0.05ppm. Symptoms: phosphorous causes tissue destruction , with disturbanxce in carbohydrate, fat, protein metabolism in the liver. Deposition ofglycogen in liver is inhibited; deposition of fat is increased. Chronic absorption of phosphorous increases bone formation under the epiphyseal cartilage and impairs blood circulation in bone by bone formation in haverian and marrow canals. These changes lead to necrosis and sequestration of bone; they occur most frequentlyu in the mandible. The pathologic findings in yellow phosphorous poisoning are jaundice, fatty degeneration and necrosis of the

Clofazimine alters the energy metabolism and inhibits the growth rate of a human lung-cancer cell line in vitro and in vivo. The anti-leprosy drug Clofazimine is known to inhibit respiratory function and hence energy metabolism in yeast and in transformed fibroblasts. The aim of this study was to examine the effect of Clofazimine on the energy metabolism of a chemoresistant human non-small-cell bronchial-carcinoma cell line (WIL) and to determine whether this agent might inhibit the growth rate of this cell line in vitro and in vivo. Oxidative phosphorylation was estimated in vitro by measuring oxygen consumption polarographically and glycolysis was estimated from lactate production. In cells that had been pre-treated with an ATP synthetase inhibitor (oligomycin), the addition of Clofazimine resulted in an increase in oxygen consumption similar to that observed with 2,4-dinitrophenol, a classical inhibitor of oxidative phosphorylation. This inhibition of mitochondrial function was ass