Effect of cisplatin and cobalt chloride on antioxidant enzymes in the livers of Lewis lung carcinoma-bearing mice: protective role of heme oxygenase.

Changes in the activities of antioxidant enzymes superoxide dismutase, catalase (CAT), glutathione peroxidase and heme oxygenase (HO) and changes in lipid peroxidation and reduced glutathione (GSH) levels were measured in the livers of control and Lewis lung carcinoma (LLC)-bearing mice 24 h after a single injection of cisplatin or CoCl(2). Treatment with cisplatin induced the same degree of lipid peroxidation and GSH depletion as did CoCl(2) but the antioxidant enzymes were differently involved in cisplatin- and cobalt-induced oxidative stress responses. In cobalt-treated mice the activities of these enzymes were either inhibited or not changed significantly and only the HO activity was increased (5-fold) as a main protective enzyme.

Enhanced heme oxygenase activity increases the antioxidant defense capacity of guinea pig liver upon acute cobalt chloride loading: comparison with rat liver.

Changes in the activity of so-called oxidative stress defensive enzymes, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and heme oxygenase, as well as changes in lipid peroxidation and reduced glutathione levels, were measured in guinea pig and rat liver after acute cobalt loading. Cobalt chloride administration produced a much higher degree of lipid peroxidation in guinea pig than in rat liver compared with the control animals. The intrahepatic reduced glutathione content in control guinea pig was higher than that in rat, but was equally decreased in both species after cobalt administration.

Heme oxygenase is the main protective enzyme in rat liver upon 6-day administration of cobalt chloride.

Changes in the activities of rat liver heme oxygenase (HO), superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione reductase (GR), as well as changes in lipid peroxidation and reduced glutathione (GSH) levels were measured after acute loading and chronic administration of cobalt chloride (CoCl2). Acute loading was achieved by a single subcutaneous injection of 60 mg CoCl2/kg body weight for 24 h. Chronic administration was performed by giving the same total amount of CoCl2 in small doses over longer periods of time: 30 mg CoCl2/kg daily for 2 days, 15 mg CoCl2/kg daily for 4 days, or 10 mg CoCl2/kg daily for 6 days.

Heme oxygenase--carbon monoxide signalling pathway as a physiological regulator of vascular smooth muscle cells.

Heme oxygenase (HO) is a microsomal enzyme involved in the degradation of heme and biliverdin and carbon monoxide, the former being subsequently converted to bilirubin by the cytosolic biliverdin reductase. Two isoenzymes transcribed from separate genes have been characterized. The HO-2 isoform is constitutively expressed and is present in high concentration in the brain and testes.

Loss of glucose transport in developing avian red cells.

Although red cells are generally associated with significant glucose transport and dependence on glycolysis, the mature red cells of some species (e.g. pig) show very low glucose transport.