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

Objective: Objective to investigate the health changes of patients with severe trimethyltin chloride (TMT) poisoning in four years. Methods: Six patients with severe TMT poisoning treated in the First Affiliated Hospital of Gannan Medical College in August 2016 were numbered 1, 2, 3, 4, 5 and 6 respectively. The patients were followed up 0.5, 2 and 4 years after poisoning and compared and analyzed. The follow-up contents include: symptom degree, score of simple mental intelligence examination scale (MMSE) and modified Rankin Scale (MRS) , cranial magnetic resonance imaging (MRI) , EEG, etc. Results: The symptoms of dizziness, headache, chest tightness, palpitation, nausea and vomiting decreased gradually in 6 patients. The symptoms of speech disorder and memory decline in No.1, 2 and 3 patients gradually increased, and the scores of MMSE and Mrs gradually decreased; Patients No.4, 5 and 6 had improved speech disorder, but their memory decreased, MMSE and Mrs scores were still flat, and mild cognitive impairment. The brain atrophy of No.1, 2 and 3 patients was aggravated, which showed obvious atrophy of hippocampus, temporal lobe, insular lobe and cerebellum and enlargement of ventricle; There was no significant change in brain atrophy in No.4, 5 and 6 patients. Conclusion: The neurotoxic symptoms in the later stage of severe TMT poisoning are still serious, and the neurotoxic time is long.
Atrophy ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Trimethyltin Compounds

Acute Disease ; Adult ; Female ; Humans ; Male ; Middle Aged ; Occupational Diseases ; chemically induced ; Trimethyltin Compounds ; poisoning

Adult ; Female ; Humans ; Occupational Diseases ; Plastics ; Trimethyltin Compounds ; poisoning ; Waste Management

China ; epidemiology ; Humans ; Occupational Diseases ; epidemiology ; prevention & control ; Surveys and Questionnaires ; Trimethyltin Compounds ; analysis ; poisoning

OBJECTIVETo investigate suitable biomarkers for workers exposure to trimethyltin chloride (TMT-cl).

METHODSUrinary samples of 44 male workers from five TMT-cl occupational poisoning incidents were collected. Methyltin mercaptide stabilizers and waste plastics used in the incidents were also collected. The levels of TMT-cl in all the samples were determined by gas chromatography. The concentration of blood potassium for each poisonings was determined compared to control group (50 male workers of a food company), and the correlation between blood potassium and urinary TMT-cl were also determined.

RESULTSTMT-cl was detected in urine of all the poisonings. The results were (0.869 +/- 0.392) microg/L (severe poisoning), (0.963 +/- 0.482) microg/L (moderate poisoning), (0.716 +/- 0.384) microg/L (mild poisoning) respectively and the difference was statistically significant (P < 0.01). But the severity of the clinical status did not seem to be closely correlated to the level of urinary TMT-cl (F = 1.88, P > 0.05). In the severe poisonings, there were no differences in urinary TMT-cl on day 4 after poisoning from day 1 (P > 0.05). In contrast, urinary TMT-cl was decreased significantly on day 4 than on day 1 in mild and moderate poisonings (P < 0.01). On day 21, levels of urinary TMT-cl of all the poisonings were higher than those of the workers exposed to TMT-cl who had no clinical status (P < 0.01). Blood potassium levels of exposed group was 77.3% which was significantly lower than normal value (P < 0.01). The concentration of blood potassium was lower than normal value (3.5 mmol/L) and was correlated with the severity of the clinical status (F = 4.45, P < 0.05). Level of urinary TMT-cl of exposed group was negatively correlated with blood potassium (r = -0.4456, P < 0.01).

CONCLUSIONLevel of urinary TMT-cl can be used as exposure biomarker of TMT-cl poisoning. Blood potassium is an early biomarker of effect for TMT-cl poisoning so as to find poisoning population early.

Adult ; Biomarkers ; blood ; urine ; Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; Potassium ; blood ; Trimethyltin Compounds ; poisoning ; urine ; Young Adult

Accidents, Occupational ; Adult ; Emergency Nursing ; Emergency Treatment ; Humans ; Male ; Poisoning ; nursing ; therapy ; Trimethyltin Compounds ; poisoning ; Young Adult

In order to the neuroprotective effect of Lycium chinense fruit (LCF), the present study examined the effects of Lycium chinense fruit on learning and memory in Morris water maze task and the choline acetyltransferase (ChAT) and cyclic adenosine monophosphate (cAMP) of rats with trimethyltin (TMT)-induced neuronal and cognitive impairments. The rats were randomly divided into the following groups: naive rat (Normal), TMT injection+saline administered rat (control) and TMT injection+LCF administered rat (LCF). Rats were administered with saline or LCF (100 mg/kg, p.o.) daily for 2 weeks, followed by their training to the tasks. In the water maze test, the animals were trained to find a platform in a fixed position during 6d and then received 60s probe trial on the 7th day following removal of platform from the pool. Rats with TMT injection showed impaired learning and memory of the tasks and treatment with LCF (p<0.01) produced a significant improvement in escape latency to find the platform in the Morris water maze at the 2nd day. Consistent with behavioral data, treatment with LCF also slightly reduced the loss of ChAT and cAMP in the hippocampus compared to the control group. These results demonstrated that LCF has a protective effect against TMT-induced neuronal and cognitive impairments. The present study suggests that LCF might be useful in the treatment of TMT-induced learning and memory deficit.
Adenosine Monophosphate ; Animals ; Choline O-Acetyltransferase ; Fruit ; Hippocampus ; Learning ; Lycium ; Memory ; Memory Disorders ; Neurons ; Neuroprotective Agents ; Rats ; Trimethyltin Compounds ; United Nations ; Water

OBJECTIVETo study the activity, protein and gene expression of renal HK-ATPase (HKA) in rats subchronic exposed to trimethyltin chloride (TMT).

METHODSIn subchronic toxic test (14-week), 55 female SD rats (age, 6 weeks) were divided randomly into 5 groups: control, low, medium, high and super high dosage, respectively, which drank water with TMT of 0, 8.20, 32.81, 131.25 and 262.50 microg x kg(-1) x d(-1) for 14 weeks. Then serum K+ levels were measured; the activities of HK-ATPase (HKA) in kidneys were detected by the method of determinated phosphorus content; Western Blot assay and real-time PCR were used to exam the protein and mRNA expression levels of HKA in kidneys, respectively.

RESULTSThe serum K+ level in super-high dosage group was (5.6 +/- 0.4) mmol/L, which was significantly lower than that [(6.9 +/- 0.3) mmol/L] in control group (P < 0.01). The HKA enzymatic activity of kidneys in low and super high dosage groups was 4.50 +/- 1.45 and 4.55 +/- 0.72 micromolPi x mg prot(-1)h(-1), respectively, which were significantly lower than that (6.55 +/- 0.77 micromol Pi x mg prot(-1) h(-1)) in control group (P < 0.05).

CONCLUSIONWhen rats were exposed subchronic to TMT, the renal HKA activity could reduce, but the expression levels of HKA protein and mRNA did not decrease.

Animals ; Female ; Gene Expression ; H(+)-K(+)-Exchanging ATPase ; genetics ; metabolism ; Kidney ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests, Subchronic ; Trimethyltin Compounds ; toxicity

OBJECTIVESTo determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia.

METHODSSD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+.

RESULTSWith increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01).

CONCLUSIONTMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.

Animals ; Female ; Hypokalemia ; chemically induced ; veterinary ; Injections, Intraperitoneal ; Kidney Diseases ; chemically induced ; veterinary ; Lethal Dose 50 ; Male ; Rats ; Rats, Sprague-Dawley ; Severity of Illness Index ; Trimethyltin Compounds ; pharmacology ; poisoning