allopurinol and Poisoning

Heavy metals become toxic when they are not metabolized by the body and accumulate in the soft tissue. Chelation therapy is mainly for the management of heavy metal-induced toxicity; however, it usually causes adverse effects or completely blocks the vital function of the particular metal chelated. Much attention has been paid to the development of chelating agents from natural sources to counteract lead- and iron-induced hepatic and renal damage. Sesame oil (a natural edible oil) and sesamol (an active antioxidant) are potently beneficial for treating lead- and iron-induced hepatic and renal toxicity and have no adverse effects. Sesame oil and sesamol significantly inhibit iron-induced lipid peroxidation by inhibiting the xanthine oxidase, nitric oxide, superoxide anion, and hydroxyl radical generation. In addition, sesame oil is a potent inhibitor of proinflammatory mediators, and it attenuates lead-induced hepatic damage by inhibiting nitric oxide, tumor necrosis factor-α, and interleukin-1β levels. Because metal chelating therapy is associated with adverse effects, treating heavy metal toxicity in addition with sesame oil and sesamol may be better alternatives. This review deals with the possible use and beneficial effects of sesame oil and sesamol during heavy metal toxicity treatment.

Topics: Benzodioxoles; Chelating Agents; Heavy Metal Poisoning; Humans; Hydroxyl Radical; Interleukin-1beta; Iron; Kidney; Lipid Peroxidation; Liver; Nitric Oxide; Phenols; Poisoning; Sesame Oil; Superoxides; Tumor Necrosis Factor-alpha; Xanthine Oxidase

To study the change in oxidase and anti-oxidase in liver of the mice poisoned by dimethylformamide (DMF), and the effects of the treatment with sulfhydryl compounds in acute poisoning of DMF.. The sulfhydryl compounds included sodium dimercaptopropane (Na-DMPS), N-acetylcysteine (NAC), glutathione (GSH) and dimercaptosuccinic acid (DMSA). The model of acute poisoning with DMF in mice was reproduced, and the left hepatic lobes were harvested at 6, 12, 24, 48 and 72 hours after DMF to detect the dynamic changes in the activities of superoxide dismutase (SOD) and xanthine oxidase (XOD) in liver homogenate. Treatment groups included intraperitoneal injection of Na-DMPS, NAC, GSH, DMSA respectively. In the control groups, the activities of XOD and SOD in liver were determined 24 hours after intragastric administration of DMF.. The activities of XOD, SOD in liver were elevated at 24 hours after intragastric administration of DMF (both P<0.01), and returned to the normal levels at 48-72 hours. Compared to the poisoning group, the activities of XOD, SOD in liver homogenate were significantly lowered after the treatment of Na-DMPS, NAC and DMSA (P<0.05 or P<0.01). The activity of XOD in liver homogenate was reduced 24 hours after treating with GSH (P<0.05), and no obvious change was observed in SOD (P>0.05). As far as the activity of SOD was concentrated, Na-DMPS, NAC, DMSA showed better effects than GSH (all P<0.05), and Na-DMPS was the best. There was no significant differences in XOD among the four sulfhydryl compounds.. The balance of oxidase and anti-oxidase is interrupted by DMF, which might be one of the mechanisms of damage to the liver. Na-DMPS, NAC and DMSA could protect liver function by restoring the balance.

Topics: Animals; Antidotes; Dimethylformamide; Disease Models, Animal; Female; Liver; Male; Mice; Mice, Inbred ICR; Poisoning; Random Allocation; Sulfhydryl Compounds; Superoxide Dismutase; Xanthine Oxidase

Molybdenum toxicity and the interactions between copper, molybdenum and sulphate are reviewed. The main signs of molybdenum poisoning are poor growth and anaemia (rat, chick, rabbit, cattle and sheep), anorexia (rat), diarrhoea and achromotrichia (cattle and sheep), joint and bone deformities (rat, rabbit, cattle), central nervous system degeneration and loss of crimp in wool (sheep). The following topics are discussed: (1) The effect of sulphate and sulphur compounds on molybdenum toxicity. (2) The effect of molybdenum on tissue copper levels. (3) The effect of molybdenum on the distribution of copper in plasma. (4) The effect of molybdenum on uptake and excretion of copper. (5) The possible existence of copper(II) molybdate in vivo. (6) The influence of molybdenum on sulphide production by ruminal micro-organisms. (7) Competition between molybdenum and sulphate in intestinal transport. (8) Interaction of sulphur with copper in vivo. (9) The possible involvement of molybdenum in gout and multiple sclerosis in humans.

Topics: Animals; Anorexia; Body Weight; Cattle; Chickens; Copper; Drug Interactions; Guinea Pigs; Molybdenum; Poisoning; Rabbits; Rats; Sheep; Species Specificity; Sulfates; Turkeys; Xanthine Oxidase

Topics: Allopurinol; Animals; Blood Pressure; Central Venous Pressure; Digitalis Glycosides; Dogs; Glucose; Heart; Heart Rate; Myocardium; Oxygen Consumption; Poisoning; Potassium

Topics: Allopurinol; Animals; Endotoxins; Female; Mice; Poisoning; Salmonella typhimurium; Time Factors; Tryptophan; Tryptophan Oxygenase