Water quality assessment and apportionment source of pollution from neighbouring rivers in the Tapeng Lagoon (Taiwan) using multivariate analysis: a case study.

Factor analysis was conducted to explain the characteristics and variation in the quality of water during the disassembly of oyster frames and fishery boxes. The result shows that the most important latent factors in the Tapeng Lagoon are the ocean factor, the primary productivity factor, and the fishery pollution factor. Canonical discriminant analysis is applied to identify the source of pollution in neighbouring rivers outside the Tapeng Lagoon. The two constructed discriminant functions (CDFs) showed a marked contribution to all the discriminant variables, and that total nitrogen, algae, dissolved oxygen, and total phosphate combined in the nutrient effect factor. The recognition capacities in these two CDFs were 95.6% and 4.4%, respectively. The water quality in the Kaoping river most strongly affected the water quality in the Tapeng Lagoon. Disassembling the oyster frames and fishery boxes improved the water quality markedly. However, environmental topographic conditions indicate that strengthening stream pollution prevention and constructing another entrance to the ocean are the best approaches for improving the quality of water in the Tapeng Lagoon by reducing eutrophication. These approaches and results yield useful information concerning habitat recovery and water resource management.

Synthesis and antibacterial evaluation of certain quinolone derivatives.

A number of 7-substituted quinolone derivatives were synthesized and evaluated for antibacterial and cytotoxic activities. Preliminary results indicated that most compounds tested in this study demonstrated better activity against methicillin-resistant Staphylococcus aureus than norfloxacin. Among them, 1-(4-amino-2-fluorophenyl)-6-fluoro-1,4-dihydro-7-[4-[2-(4-methoxyphenyl)-2-hydroxyiminoethyl]-1-piperazinyl]-4-oxo-3-quinolinecarboxylic acid (11d) and its ketone precursor 10d exhibited significant activities against Klebsiella pneumoniae, methicillin-resistant S. aureus, erythromycin- and ampicillin-resistant Streptococcus pneumoniae, and vancomycin-resistant Enterococcus faecalis. Due to strong cytotoxicities of 11d (a mean log GI(50) of -5.40), compound 10d, with good antibacterial activities and low cytotoxicities (a mean log GI(50) of -4.67), is a more potential drug candidate.

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.

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 consecutive 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.

Differential patterns of ERK and STAT3 phosphorylation after sciatic nerve transection in the rat.

Peripheral nerve injury induces a specific pattern of expression of growth factors and cytokines, which regulate injury responses and regeneration. Distinct classes of growth factors and cytokines signal through specific intracellular phosphorylation cascades. For example, the ERK phosphorylation cascade mediates signaling through transmembrane tyrosine kinase receptors and the JAK/STAT cascade mediates signaling through the GP130 receptor complex. We tested whether specific phosphorylation patterns of ERK and STAT3 result from nerve injury and whether such phosphorylation correlates with the expression of specific growth factors and cytokines. At sites adjacent to a nerve transection, we observed that ERK phosphorylation peaked early, persisted throughout 16 days, and was equally intense at proximal and distal sites. In contrast, STAT3 phosphorylation peaked later than ERK but did not persist as long and was stronger in the proximal than in the distal segment adjacent to the injury. In addition, in distal segments further away from the injury site, ERK became phosphorylated with a delayed time course, while STAT3 remained unphosphorylated. These patterns of phosphorylation correlated well with the expression of neurotrophin and interleukin-6 mRNAs in the distal stump. In addition, we found that the pattern of SAPK phosphorylation is similar to the pattern observed for STAT3, while the pattern of macrophage infiltration into the transected nerve was distinct from all the phosphorylation patterns observed. Together, these observations suggest that ERK activation is important in the establishment of a regeneration-promoting extracellular environment in the far distal stump of transected nerves and that STAT3 activation is important in the control of cellular responses close to the site of injury.

Synthesis, antibacterial, and cytotoxic evaluation of certain 7-substituted norfloxacin derivatives.

We report herein the synthesis and biological evaluation of two series of 7-substituted norfloxacin derivatives. Most compounds tested in this study demonstrated better activity against methicillin-resistant Staphylococcus aureus than norfloxacin. Preliminary in vitro evaluation indicated that the 7-[4-(2-hydroxyiminoethyl)piperazin-1-yl] derivatives 3b-e possess distinct cytotoxicity profiles as compared with their alpha-methylene-gamma-butyrolactone counterparts, 4b,e: i.e., excellent activities against the renal cancer subpanel. Among them, 1-ethyl-6-fluoro-7-¿4-[2-(4-chlorophenyl)-2-hydroxyiminoethyl]-1-p ipe razinyl¿-4-oxo-1,4-dihydro-3-quinolinecarboxylic acid (3d) demonstrated the most significant activities against renal cancer cell lines, with log GI(50) values of -6.40 against CAK-1, -6.14 against RXF 393, and -7.54 against UO-31, compared with a mean log GI(50) value of -5.03.

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 microg 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.

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.

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 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.

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.

[The effects of exercise on the arterial potassium and ventilatory response under hyperoxic, normoxic, and hypoxic conditions].

BACKGROUND: Exercise leads to an increase in plasma potassium, the animal experiments showed that potassium infusion stimulated ventilation and abolished by peripheral chemodenervation and also showed that combined effects of potassium and hypoxia were greater than the sum of the individual effects. This study proposed to investigate plasma potassium and its correlation with exercise, and to investigate the effects of hypoxia and hyperoxia on potassium and ventilation during steady state exercise. METHODS: Ten male subjects exercised on a cycle ergometer. Each performed (1) incremental exercise test; (2) steady state exercise test with a work rate of about 75% of anaerobic threshold under hyperoxic (FiO2 100%), normoxic (FiO2 21%) and hypoxic (FiO2 12%) conditions, respectively. RESULTS: Arterial plasma potassium concentration rose from a pre-exercise level of 3.97 +/- 0.40 mEq/L to the post-exercise level of 5.11 +/- 0.49 mEq/L. The increase in plasma potassium during exercise correlated well with the increase in lactate (r = 0.72, p < 0.05) and the decrease in pH (r = 0.69, p < 0.05). During the steady state exercise test, switching the subject from room air to hypoxic (12% O2) conditions led to a significant rise in both plasma potassium (p < 0.05) and ventilation (p < 0.05) with good correlation between the potassium increase and the increase in ventilation (r = 0.85, p < 0.05). Switching the subject from room air to hyperoxic (100% O2) condition resulted in a significant decrease in ventilation (p < 0.05) without significant change in plasma potassium (p > 0.01). CONCLUSIONS: It was concluded that (1) exercise can lead to an increase in arterial potassium, hydrogen ion, lactate in men; (2) hypoxia can stimulate the peripheral chemoreceptor and increase plasma potassium level. Potassium may, therefore, be an important factor by which the magnitude of the peripheral chemoreflex response is augmented during exercise.

Changes of lipase-catalyzed lipolytic rates in a batch reactor.

A dramatic change of the reaction rate was observed for the lipase-catalyzed hydrolysis of tributyrin in a batch reactor. Immediately after the addition of the enzyme, the lipolysis rate increased continuously until a maximal reaction rate was reached. The duration of the induction was mainly controlled by the bulk enzyme concentration and the reactor stirring speed. The reaction rate dropped sharply after reaching its maximal value. The lipolysis decayed at a rate of about 0.012 min(-1), and was not affected by changes of the stirring speed. This decay was attributed to the fast deactivation of the surface-adsorbed lipase, and possibly to the extremely slow desorption of the inactivated species. For reaction time longer than 120 minutes, the lipolysis decreased at a much slower rate. Several mechanisms for the decay of the lipolysis rate were discussed.