Jenn-Yuan Sheu

Association between oxidative stress and changes of trace elements in patients with breast cancer.

OBJECTIVES To investigate the association between oxidative stress and certain trace elements in the blood of breast cancer patients. DESIGN AND METHODS Malondialdehyde (MDA) was measured in serum of patients with breast cancer (n = 35) and controls (n = 35) by high performance liquid chromatography. Trace elements were determined by atomic absorption spectrophotometry. RESULTS In the present study, significantly increased lipid peroxidation, measured as MDA, was demonstrated in the serum of breast cancer patients (p < 0.01). The concentrations of zinc and iron remained unaltered. However, the mean serum copper level in patients with breast cancer was significantly higher than the control group (p < 0.01). In addition, the mean serum selenium level in patients with stage III was significantly lower than the control group (p < 0.05). Moreover, a positive correlation was also observed between copper and MDA levels in the patient group but not in the control group. CONCLUSION In the present study, the presence of an association between oxidative stress and trace elements was observed in patients with breast cancer. We suggest that increased oxidative stress in patients with breast cancer may result from changes in the levels of certain trace elements.

Cadmium-induced renal lipid peroxidation in rats and protection by selenium.

Cadmium has been recognized as one of the most toxic environmental and industrial pollutants. The kidney is a critical target organ following Cd exposure. The aim of this study was to investigate the effects of cadmium-induced peroxidative damage to rat kidney. Treatment of rats with Cd resulted in a time- and dose-related accumulation of metal in kidney. Cd produced enhanced lipid peroxidation in plasma and kidney. These Cd-induced changes were accompanied by a significant rise in renal Fe and Cu, and a fall in tissue Zn and Se. Concurrent treatment with Se and Cd reduced the Cd-induced alterations in renal peroxidation and essential metal levels. Data suggest that lipid peroxidation is associated with Cd toxicity and that Se was found effective in attenuation of these renal effects.

Cadmium induced lipid peroxidation in rat testes and protection by selenium.

The main goal of this study was to investigate the role of cadmium in the promotion of lipid peroxidation in the homogenates of rat testes and the effect of selenium on lipid peroxidation in testes of rats after cadmium injection. Treatment of rats with cadmium resulted in a time- and dose-related accumulation of the metal ions in testes. The concentrations of cadmium, copper, zinc, selenium and iron in the tissues were determined by an atomic absorption spectrophotometer and lipid peroxidation in testes was measured by a spectrophotometer. Cadmium produced enhanced lipid peroxidation in testes. These cadmium-induced changes were accompanied by a significant increase of iron and copper, and a decrease of zinc in testes. Concurrent treatment with selenium and cadmium reduced the cadmium-induced alterations in lipid peroxidation and essential metal levels. Data suggest that lipid peroxidation was associated with cadmium toxicity in testes and that the addition of selenium was found to be effective in attenuation of this effect.

Cadmium-induced liver, heart, and spleen lipid peroxidation in rats and protection by selenium

The purpose of this study was to evaluate the effects of cadmium-induced peroxidative damage to rat liver, heart, and spleen. Sprague-Dawley rats were injected subcutaneously with a single dose of 25, 125, 500, or 1250 µg Cd/kg and evaluated 6, 12, 24, or 72 h later. Liver, heart, and spleen were analyzed for lipid peroxidation and Fe, Cu, Zn, Se, and Cd concentrations. Data showed that Cd produced enhanced lipid peroxidation in the liver, heart, and spleen. These Cd-induced changes were accompanied by a significant rise in liver, heart, and spleen Fe and Cu, and a fall in spleen Zn and liver, heart, and spleen Se. Concurrent treatment with Se and Cd reduced the Cd-induced alterations in liver, heart, and spleen peroxidation and essential metal levels. Data suggest that lipid peroxidation is associated with cadmium toxicity and that Se was found effective in preventing lipid peroxidation.

LIPID PEROXIDATION IN WORKERS EXPOSED TO HEXAVALENT CHROMIUM

The aim of this study was to investigate whether exposure to hexavalent chromium induces lipid peroxidation in human. This study involved 25 chrome-plating factory workers and a reference group of 28 control subjects. The whole-blood and urinary chromium concentrations were determined by graphite furnace atomic absorption spectrophotometry. Malondialdehyde (MDA), the product of lipid peroxidation, was determined by high-performance liquid chromatography, and the activities of protective enzymes were measured by ultraviolet-visible spectrophotometry. In the chrome-plating workers, the mean concentrations of chromium in blood and urine were 5.98 microg/L and 5.25 microg/g creatinine, respectively; the mean concentrations of MDA in blood and urine were 1.7 micromol/L and 2.24 micromol/g creatinine. The concentrations of both chromium and MDA in blood and urine were significantly higher in the chromium-exposed workers. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) were not markedly different between control and exposed workers. Data suggest that MDA may be used as a biomarker for occupational chromium exposure. Antioxidant enzymic activities are not a suitable marker for chromium exposure.

OXIDATIVE EFFECTS OF NICKEL ON BONE MARROW AND BLOOD OF RATS

This study was undertaken to examine the oxidative effects of nickel (Ni) on rat blood and bone marrow. Treatment with either 100, 250, or 500 micromol/kg Ni i.p. significantly enhanced lipid peroxidation in serum and bone marrow after 24 h. The concentrations of Ni and Fe in serum and bone marrow cells were also significantly increased after NiCl2 administration. After treatment with NiCl2, the activities of glutathione peroxidase (GPx) and levels of alpha-tocopherol in bone marrow cells were markedly reduced. There was an inverse association thiobarbituric acid elevated (TBA)-chromogen product with decreased GPx activity and alpha-tocopherol levels in bone marrow cells of NiCl2-treated rats. The concentrations of alpha-tocopherol in blood significant reduced with 100 and 250 micromol/kg Ni but returned to control at the 500-micromol/kg dose. Data suggest that lipid peroxidation may be a contributing factor in Ni-induced tissue oxidative stress.

Lipid peroxidation in rat adrenal glands after administration cadmium and role of essential metals

The aim of this study was to investigate the effects of cadmium-induced peroxidative damage to rat adrenals. Cadmium significantly increased adrenal lipid peroxidation in a dose- and time-related manner. Cadmium-induced lipid peroxidation was accompanied by a marked elevation in adrenal iron (Fe) levels, in particular the free elemental form. Chelation of Fe with deferoxamine decreased the cadmium effect on lipid peroxidation. Selenium (Se) was also effective in inhibiting Cd-induced adrenal lipid peroxidation. Data indicate that Cd-induced lipid peroxidation in rat adrenals may be dependent upon Fe and Se levels in this tissue.

BRAIN LIPID PEROXIDATION AND CHANGES OF TRACE METALS IN RATS FOLLOWING CHRONIC MANGANESE CHLORIDE EXPOSURE

The aim of this study was to investigate the effects of chronic, daily, 30-d administration of manganese chloride (MnCl 2 ) to male Sprague-Dawley rats on lipid peroxidation and changes of trace elements (manganese, iron, copper, zinc) in various brain regions. Rats were intraperitoneally injected with MnCl 2 (20 mg/kg) once daily for 30 consecutive days. The Mn accumulated in frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus, medulla, cerebellum, and spinal cord. Malondialdehyde, an end product of lipid peroxidation, was markedly decreased in frontal cortex and cerebellum. An increased level of Cu was observed in frontal cortex, medulla, and a cerebellum. A decreased Fe level was found only in cerebellum, and a decreased Zn level was observed in hippocampus and striatum. In a second group of animals, Mn (20 mg/kg/d) and glutathione (GSH, 15 mg/kg/d) were administered ip for 30 d. In GSH-Mn-treated rats, compared to Mn-treated rats, MDA concentrations were significantly reduced in frontal cortex, medulla and cerebellum. The changes of trace elements in rat brain were similar to the Mn-treated group. We suggest that Mn is an atypical antioxidant, as well as not involved in oxidative damage in rat brain. Fe and Cu may play roles in the protective effect of Mn against lipid peroxidation in rat brain.

Protective effects of manganese against lipid peroxidation.

The aim of this study was to investigate the effects of chronic, daily, 30-d administration of manganese chloride (MnCl2) to male Sprague-Dawley rats on lipid peroxidation in various tissues. Rats were intraperitoneally injected with MnCl2 (20 mg/kg) once daily for 30 con secutive days. The Mn accumulated in liver, spleen, adrenal glands, heart, kidneys, lung, and testes. This was associated with decreased lipid peroxidation in liver, spleen, and adrenal glands and a decrease in the levels of Fe in these tissues. In a second group of animals, Mn (20 mg/kg/d) and glutathione (GSH, 15 mg/kg/d) were administered ip for 30 d. GSH counteracted the Mn-induced protective fall in lipid peroxidation, but Fe levels remained lower in liver and spleen. Mn decreases lipid peroxidation in certain tissues, which may involve lowering Fe content, but interaction with Fe is not the sole mechanism.