Alloys ; toxicity ; Cobalt ; toxicity ; Lung ; Lung Diseases ; diagnosis ; therapy ; Tungsten ; toxicity

Alloys ; toxicity ; Cobalt ; toxicity ; Humans ; Lung Diseases ; chemically induced ; Tungsten ; toxicity

Cobalt or chromium alloys are the most common clinical materials of prosthesis and there have been some investigators at home and abroad have done related researches about the genotoxic effects of cobalt and chromium ions and nanoparticles. People have certain understanding about the mechanism of production of ions as well as their influence on cells. However, chromium or cobalt nanoparticles genotoxicity related research is still in its preliminary stage. In each stage, the mechanisms, from creating of the particles, through entering cells, until finally causing genotoxic, are still contained many problems to be solved. This article reviews the research progress in mechanisms of production and genotoxic effects of cobalt, chromium ions and nanoparticles.
Chromium ; toxicity ; Cobalt ; toxicity ; DNA Damage ; Humans ; Ions ; Nanoparticles ; toxicity ; Prostheses and Implants

Cobalt/toxicity* ; Computational Biology ; Kidney/drug effects* ; Kidney Diseases/genetics* ; Humans

BACKGROUNDGiant cell interstitial pneumonia (GIP) was a rare form of pneumoconiosis, associated with exposure to hard metals, which had been reported mostly as isolated case reports. We described eight cases of GIP diagnosed in our hospital during the past seven years, with particular reference to new findings.

METHODSEight patients with GIP confirmed by biopsy in the Nanjing Drum Tower Hospital affiliated to Medical School of Nanjing University from 2005 to 2011 were retrospectively analyzed. For each patient, the occupy histories and medical records were thoroughly reviewed and clinic data were extracted. Two radiologists, without knowledge of any of the clinical and functional findings, independently reviewed the HRCT scans of all patients. Follow-up data were collected.

RESULTSAmong the eight patients, seven had a history of exposure to hard metal dusts, one denied an exposure history. The most common manifestations were cough and dyspnea. One patient initiated with pneumothorax and another pleural effusion, both of which were uncommon to GIP. The main pathologic appearances were the presence of macrophages and multinucleated giant cells in the alveolar space. The clinical symptoms and radiographic abnormalities were obviously improved after cessation of exposure and receiving corticosteroid treatments, recurrences were observed in two patients when they resumed work. In spite of exposure cessation and corticosteroid treatment, one patient developed pulmonary fibrosis at seven years follow-up.

CONCLUSIONSAwareness of the patients' occupational history often provided clues to the diagnosis of GIP. Histopathologic examinations were necessary to establish the right diagnosis. Exposure cessation was of benefit to most patients; however, pulmonary fibrosis was possible in spite of exposure cessation and corticosteroid treatment. Better ways should be found out to improve the outcome and quality of life.

Adult ; Alloys ; toxicity ; Cobalt ; toxicity ; Female ; Humans ; Lung ; pathology ; Lung Diseases, Interstitial ; diagnosis ; etiology ; Male ; Middle Aged ; Pulmonary Fibrosis ; diagnosis ; etiology ; Retrospective Studies ; Tungsten ; toxicity ; Young Adult

OBJECTIVETo study the sensitivity of Jatropha curcas seeds from three different locations to (60)Co-gamma radiation and to determine the medial lethal doses (LD50) of (60)Co-gamma radiation for these seeds.

METHODSSix different radiation doses (0, 100, 150, 200, 250 and 300 Gy) were used. Based on the germination rate 50%, LD50 doses of (60)Co-gamma radiation for the seeds were calculated using linear regression equation.

RESULTSLD50 doses of (60)Co-gamma radiation for these seeds were 178 Gy (seeds from Guangdong), 132 Gy (seeds from Hainan) and 198 Gy (seeds from India) respectively. Increasing radiation doses caused more significant changes in leaf shape of the M1 seedlings.

CONCLUSIONThe results provides an important experimental basis for the radiation breeding of the important herbal and energy plant J. curcas.

Cobalt Radioisotopes ; toxicity ; Gamma Rays ; Germination ; radiation effects ; Jatropha ; radiation effects ; Lethal Dose 50 ; Seeds ; radiation effects

OBJECTIVETo determine the effects of water hardness on the toxicities of cobalt (Co) and nickel (Ni) to a freshwater fish, Capoeta fusca.

METHODSToxicity was investigated by static bioassay. Fish were exposed to cobalt (as CoCl(2)) and nickel (as NiCl(2)) for 96 h in waters with two levels of hardness ("hard" and "very hard", nominally 130 mg/L and 350 mg/L as CaCO(3), respectively).

RESULTSWater hardness had a significant effect on the acute toxicity of both elements. The 96 h LC(50) values for Co were 91.7 mg/L and 204.8 mg/L in hard and very hard waters, respectively, and for Ni the 96 h LC(50) values were 78.0 mg/L and 127.2 mg/L, respectively.

CONCLUSIONThe fish were more sensitive to Co and Ni toxicity in hard water than in very hard water; very hard water protects C. fusca against the toxicity of Co and Ni.

Animals ; Calcium Carbonate ; analysis ; Cobalt ; analysis ; toxicity ; Cyprinidae ; growth & development ; Environmental Monitoring ; Fresh Water ; analysis ; Iran ; Lethal Dose 50 ; Nickel ; analysis ; toxicity ; Toxicity Tests, Acute ; Water Pollutants, Chemical ; analysis ; toxicity

Ligustrazine, one of the major effective components of the Chinese traditional medicinal herb Ligusticum Chuanxiong Hort, has been reported plenty of biological activities, such as protect cardiovascular and cerebrovascular, neuroprotection and anti-tumor, et al. Because of its remarkable effects, studies on structural modification of ligustrazine have attracted much attention. Ligustrazine synthetic derivatives reported in recent decades are mainly derived from four primary intermediates (TMP-COOH, TMP-OH, TMP-NH2, HO-TMP-OH). To explore the neuroprotection activitiy of ligustrazine intermediates, six ligustrazine intermediates (2, 5, 8, 11, 12, 13) were synthesized and their protective effects against CoCl2-induced neurotoxicity in differentiated PC12 cells were studied. The target compounds were prepared via different chemical methods, including oxidation, substitution, esterification and amidation without changing the structure nucleus of ligustrazine. Compared with TMP (EC50 = 56.03 micromol x L(-1)), four compounds (2, 5, 12 and 13) exhibited higher activity (EC50 < 50 micromol x L(-1)) respectively, of which, compound 2 displayed the highest protective effect against the damaged PC12 cells (EC50 = 32.86 micromol x L(-1)), but target compounds 8 and 11 appeared lower activity (EC50 > 70 micromol x L(-1)). By structure-activity relationships analysis, the introduction of carboxyl, amino to the side chain of ligustrazine and appropriately increase the proportion of ligustrazine may contribute to enhance its neuroprotective activity, which provides a reference for the design, synthesis and activity screening of relevant series of ligustrazine derivatives in the future.
Animals ; Cell Differentiation ; drug effects ; Chemistry Techniques, Synthetic ; Cobalt ; toxicity ; Drugs, Chinese Herbal ; chemistry ; Neuroprotective Agents ; chemical synthesis ; chemistry ; pharmacology ; Neurotoxins ; toxicity ; PC12 Cells ; Pyrazines ; chemical synthesis ; chemistry ; pharmacology ; Rats

OBJECTIVETo investigate the neuroprotective effects and mechanism of hyperin on CoCl2-induced hypoxic/ischemic PC12 cells.

METHODCoCl2 was used to treat rat pheochromocytoma cell line (PC12) to investigate the protective effects of different concentrations of hyperin.

RESULTHyperin could significantly inhibit CoCl2-induced cytotoxicity and apoptosis on PC12 cells in a dose-dependent manner, by inhibiting reactive oxygen species (ROS) production, increasing mitochondrial membrane potential (MMP), and inactivating caspase-3 and poly ADP-ribose polymerase (PARP).

CONCLUSIONHyperin could inhibit CoCl2-induced cytotoxicity and apoptosis on PC12 cells, show neuroprotective effects on hypoxic/ischemic neural injuries.

Animals ; Apoptosis ; drug effects ; Cell Survival ; drug effects ; Cells ; cytology ; drug effects ; Cobalt ; toxicity ; Hypericum ; chemistry ; PC12 Cells ; Plant Extracts ; pharmacology ; Protective Agents ; pharmacology ; Quercetin ; analogs & derivatives ; pharmacology ; Rats

OBJECTIVETo investigate the neuroprotective effects of edaravone (Eda) on cobalt chloride (CoCl2)-induced oxidative stress and apoptosis in cultured PC12 cells as well as the underlying mechanisms.

METHODSPC12 cells impaired by CoCl2 were used as the cell model of hypoxia. MTT (methyl thiazolyl tetrazolium) was used to assay the viability of the PC12 cells exposed to Eda with gradient concentrations; Hochest 33258 stain assay was used to analyze the apoptosis ratio of the PC12 cells; Bcl-2 and Bax protein levels in PC12 cells were examined by western blotting. ROS level, the mitochondrial transmembrane potential and caspase-3 activity in each group were detected by spectrofluorometer.

RESULTSCoCl2 treatment caused the loss of cell viability in PC12 cells, which was associated with the elevation of apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. CoCl2 also significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, Eda significantly reversed these phenotypes, with its maximum protective effect at 0.1 micromol/L.

CONCLUSIONThese results indicated that Eda could protect PC12 cells from CoCl2-induced cytotoxicity, and this protection might be ascribed to its anti-oxidative and anti-apoptotic activities.

Animals ; Antimutagenic Agents ; toxicity ; Antipyrine ; analogs & derivatives ; pharmacology ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Count ; methods ; Cell Survival ; drug effects ; Cobalt ; toxicity ; Dose-Response Relationship, Drug ; Drug Interactions ; Free Radical Scavengers ; pharmacology ; Membrane Potential, Mitochondrial ; drug effects ; PC12 Cells ; drug effects ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Reactive Oxygen Species ; metabolism ; bcl-2-Associated X Protein ; metabolism