OBJECTIVETo investigate the effects of tributyltin chloride (TBT) and triphenyltin chloride (TPT) on rat testicular Leydig cells.

METHODSThe rat Leydig cells (LC-540) were incubated with 0 to 80 nmol/L TBT and TPT for 24 to approximately 96 h, and then the cell viability was determined by MTT. DNA fragmentation ladder formation of cell apoptosis was examined by agarose electrophoresis. Effects of chelator of intracellular Ca2+ (BAPTA) and the inhibitors of PKA, PKC and TPK on cell apoptosis induced by TBT were observed. Effects of TBT on testosterone production in primary cultured rat Leydig cells treated with or without hCG were detected.

RESULTSTBT and TPT suppressed Leydig cell survival in a time- and dose-dependent manner. The suppressive effects of TBT and TPT on the cell survival was caused by apoptosis which was determined by DNA ladder formation. The apoptotic effect of TBT was possibly mediated by the rise in intracellular Ca2+ because it could be blocked by BAPTA, the chelator of intracellular Ca2+; PKA, PKC and TPK inhibitors did not prevent the apoptotic effects induced by TBT. TBT markedly suppressed testosterone production of primary cultured rat Leydig cells with or without hCG stimulation.

CONCLUSIONTBT and TPT induced apoptosis in rat testicular Leydig cells possibly through increasing intracellular Ca2+. TBT reduced the testosterone production of rat Leydig cells.

Animals ; Apoptosis ; drug effects ; Calcium ; metabolism ; Cell Line ; Dose-Response Relationship, Drug ; Environmental Pollutants ; toxicity ; Leydig Cells ; drug effects ; metabolism ; secretion ; Male ; Organotin Compounds ; toxicity ; Rats ; Testosterone ; secretion ; Trialkyltin Compounds ; toxicity

AIMThe interactions between diorganotin (IV) complexes of 1,3-dimethyl-4-acetyl-5-pyrazolone (HL1) and mono-nucleotides together with DNA near physiological condition were investigated.

METHODSThe mode of action of the diorganotin (IV) complexes with mononucleotides and DNA under different conditions and different times were investigated by high resolution NMR technology and UV spectra.

RESULTSThe interaction of [(L1)2SnEt2] with AMP was shown to result in significant change of chemical shift of H(8), H(2) and 31P of AMP. Hyperchromic effect of DNA could be observed due to the interaction of; [(L1)2SnEt2] with DNA, while interaction of [(L1)2SnMe2] with AMP and DNA could only cause obvious change of chemical shift of 31P and lead to hypochromic effect of DNA.

CONCLUSIONThe results indicate that [(L1)2SnEt2] can selectively bind to the N1 atom of the base and the phosphate oxygen atom of AMP and may further destroy the helical structure of DNA, while the dimethyltin (IV) compound of 1,3-dimethyl-4-acetyl-5-pyrazolone [(L1)2SnMe2] merely binds to the the phosphate oxygen atom of AMP and causes the contraction of DNA helical structure.

Antineoplastic Agents ; chemistry ; DNA ; chemistry ; Nucleotides ; chemistry ; Organotin Compounds ; chemistry ; Porphyrins ; chemistry

Adult ; Arsenic Poisoning ; etiology ; Female ; Humans ; Male ; Middle Aged ; Organotin Compounds ; poisoning ; Water Pollution ; Young Adult

Acute Disease ; Adult ; Humans ; Male ; Middle Aged ; Organotin Compounds ; poisoning ; Retrospective Studies

Accidents, Occupational ; Adolescent ; Adult ; Humans ; Male ; Middle Aged ; Organotin Compounds ; poisoning ; Young Adult

Adolescent ; Adult ; Female ; Humans ; Male ; Occupational Exposure ; Organotin Compounds ; poisoning ; Poisoning ; diagnosis ; therapy ; Retrospective Studies ; Young Adult

BACKGROUND: Although organotin compounds are widely used as PVC stabilizers, catalysts and biocides, their effects on humans are not well known. However, their acute intoxication is known to cause neurotoxicity in the central nervous system, renal toxicity, and hepatotoxicity. As there has been no previously published case of organotin intoxication in Korea, we report here the first Korean case of acute exposure to organotin. CASE REPORT: A 43-year-old male with disorientation and behavioral change was admitted to a hospital. He had been working as a tank cleaner for several different companies in the previous 8 years and a week before admission, he had cleaned a tank containing dimethyltin (DMT) for 4 days. A day after finishing the job, he suffered decreased memory, behavioral change and progressive mental deterioration when he arrived at the emergency room. The result of spinal tapping was negative but on the 4th day of admission he deteriorated into a state of coma along with metabolic acidosis and severe hypokalemia. High levels of DMT and trimethyltin (TMT) were detected in a highly sensitive urine analysis. After conservative treatment and chelation therapy, the patient showed some clinical improvement but the neurological defects persisted. CONCLUSION: The patient appeared to have been intoxicated from the acute exposure to a high level of organotin while cleaning the tank.
Acidosis ; Adult ; Central Nervous System ; Chelation Therapy ; Coma ; Disinfectants ; Emergency Service, Hospital ; Humans ; Hypokalemia ; Korea ; Male ; Memory ; Organotin Compounds ; Poisoning* ; Spinal Puncture

PURPOSE: Because previous studies have reported depleted antioxidant capacity in patients with chronic pancreatitis (CP), prevention of free radical production has gained importance in antifibrotic treatment strategies for CP. The aim of this study was to investigate the effects of ascorbic acid on oxidative capacity and pancreatic damage in experimental CP. MATERIALS AND METHODS: CP was induced in male Sprague-Dawley rats by infusion of dibutyltin dichloride (DBTC) into the tail vein. Ascorbic acid was given intraperitoneally at a daily dose of 10mg/kg body weight. The treatment groups were as follows: group 1, DBTC plus intraperitoneal physiologic saline; group 2, DBTC plus intraperitoneal ascorbic acid; group 3, solvent plus intraperitoneal physiologic saline; group 4, no operation plus intraperitoneal physiologic saline. Each group contained 15 animals. Treatment was started after CP was established. After 4 weeks of treatment, serum hyaluronic acid and laminin levels were determined by radioimmunoassay, pancreatic tissue oxidative stress was analyzed, and the degree of pancreatic damage was determined. RESULTS: Ascorbic acid treatment markedly increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) concentrations in pancreatic tissue (p < 0.01 for both). Significant serum hyaluronic acid and laminin reductions were observed in group 2 as compared with group 1 (p < 0.05). However, the serum hyaluronic acid and laminin levels remained elevated when compared with those of groups 3 and 4 (p < 0.05). Histopathologic scores were also lower in animals with CP that underwent ascorbic acid-treatment (p < 0.05). CONCLUSION: Ascorbic acid treatment alleviated the degree of oxidative stress and pancreatic damage in rat CP. Antioxidant treatment might be considered a potential option to improve the pathologic process in CP.
Animals ; Antioxidants/pharmacology ; Ascorbic Acid/*pharmacology ; Hyaluronic Acid/blood ; Laminin/blood ; Male ; Organotin Compounds ; Oxidative Stress/drug effects ; Pancreas/*drug effects/pathology ; Pancreatic Diseases/blood/chemically induced/*prevention & control ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the role and mechanism of oxidative inflammatory cascade in pancreatic fibrosis progression of chronic pancreatitis (CP) in mice induced by dibutyltin dichloride (DBTC) plus ethanol.

METHODSThirty-six KM mice were randomly divided into 2 groups (n = 18): control group and model group (DBTC combined with ethanol). The mice in model group were intravenously injected with DBTC (8 mg/kg) in tail vein and drink 10% ethanol. After modeling 2 weeks, 4 weeks and 8 weeks, the mice were anesthetized and sacrificed, the pathological changes and the degree of fibrosis in the pancreas were observed by HE and Masson staining, the F4/80 expression level were detected by immunohistochemistry, the content of superoxide dismutase (SOD), malondialdehyde(MDA) and myeloperoxidase (MPO) were measured in the pancreatic homogenates.

RESULTSThe fibroblasts and macrophages (f4/80 positive staining) could be seen obviously in pancreas of model group at 2 weeks. At 4 weeks and 8 weeks, macrophages infiltration increased and pancreatic tissue was substituted by the proliferation of fibrosis significantly. At every time-point, in pancreatic homogenates SOD was decreased, MDA and MPO markedly increased. There was significant differences between two groups (P < 0.05).

CONCLUSIONDBTC injection joint ethanol drinking can successfully establish the model of chronic pancreatitis and pancreatic fibrosis in mice. Oxidative inflammatory cascade plays an important role in the progression of pancreatic fibrosis.

Animals ; Disease Progression ; Ethanol ; adverse effects ; Fibrosis ; Immunohistochemistry ; Malondialdehyde ; metabolism ; Mice ; Organotin Compounds ; adverse effects ; Oxidative Stress ; Pancreas ; pathology ; Pancreatitis, Chronic ; chemically induced ; physiopathology ; Peroxidase ; metabolism ; Superoxide Dismutase ; metabolism

OBJECTIVETo establish a detection method for trimethyltin chloride in urine by the Head space-GC.

METHODAfter derivatizing trimethyltin chloride, the urines was separated by the head space-gc, and then the trimethyltin chloride detected qualitatively and quantificationally.

RESULTSIn the concentration range of 0.02 ∼ 0.40 mg/L urinary trimethyltin chloride, showed a quadratic, r = 0.9992, detection limit was 0.005 mg/L, the relative standard deviation was 1.9% ∼ 2.5%, recovery was 92.0% to 100%, the urine samples can be saved at least 90 days in -18°C refrigerator.

CONCLUSIONThe instrument, reagents involved in the detection require low, the operations to processing samples are simple, high sensitivity, less interference, good reproducibility, and suitable for quantitative and qualitative analysis, convenient to promotion.

Chromatography, Gas ; methods ; Humans ; Trimethyltin Compounds ; urine ; Urinalysis ; methods