[Rat kidney mitochondrial damage induced by acute cadmium administration].

OBJECTIVE: To evaluate effect of acute cadmium administration on mitochondria from rat kidney. METHODS: 24 male Sprague-Dawley (SD) rats were randomly divided into four groups. Four groups of rats were injected with saline, 0.6, 1.2, and 1.8 mg/kg weight subcutaneously, once daily, for 5 days, respectively. Ultrastructural change of rat kidney mitochondria was observed, and respiration function, membrane potential, mitochondria swelling, and superoxide level were determined. RESULTS: Ultrastructural changes included matrix vacuolation, swelling and condensation of mitochondria. In group of 1.8 mg/kg body weight, the oxygen consumption rate during state 3 respiration [(6.25 +/- 0.61) nmol/L O2 x min(-1) x mg(-1)] and RCR value (2.45 +/- 0.23) were significantly lower than those of control group [(9.66 +/- 1.16) nmol/L O2 x min(-1) x mg(-1)] (P < 0.05), indicating respiration inhibition. The membrane potential and superoxide level of the same group were 85.89% +/- 3.82% and 116.33% +/- 3.06% of control values (P < 0.05), respectively. CONCLUSIONS: Acute cadmium administration can cause rat kidney mitochondrial damage in a dose-effect manner, including inhibition of respiration, dissipation of membrane potential, swelling of mitochondria matrix. Such damage might be related to the increase of mitochondrial free radical.

[Risk assessment of nerve conduction velocity in workers exposed to lead].

OBJECTIVE: To explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure. METHODS: The external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.3.3). The BMDL in terms of blood lead and urine lead was calculated. RESULTS: There was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively. CONCLUSION: The internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.

[Risk assessment of renal dysfunction caused by occupational lead exposure].

OBJECTIVE: To assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation. METHODS: The workers in a battery factory were selected as the subjects for the exposure and effect assessment. The occupational environmental monitoring data was collected and used to calculate the total external dose of lead. The relationship between external dose and internal dose of lead was analyzed. The external dose, blood lead (BPb) and urinary lead (UPb) were used as exposure biomarkers while the urinary N-acetyl-D-glucosaminidase (UNAG), and urinary albumin (UALB) were used as the effect biomarkers for the renal dysfunction caused by lead. Software of BMDS (BMDS 11311) was used to calculate BMD. RESULTS: The external and internal does of lead was positively correlated (BPb: r = 0.466, P < 0.01; UPb: r = 0.383, P < 0.01). The levels of BPb, UPb in exposure group (654.03 microg/L, 143.45 microg/g Cr) were significantly higher than those in the control group (57.12 microg/L, 7.20 microg/g Cr), so were UALB, UNAG; in addition, all of them presented significant dose-response relationship. The BPb BMD of UALB, UNAG were 607.76, 362.56 microg/L respectively and the UPb BMD of UALB, UNAG were 117.79, 78.79 microg/gCr respectively. CONCLUSION: Occupational lead exposure can cause renal dysfunction, which presents dose-response relationship; the risk assessment of renal dysfunction caused by occupational lead exposure is performed by BMD calculation of BPb and UPb.

[Preparation of five ginkgolic acid monomers and their molluscicidal effects against Oncomelania hupensis].

OBJECTIVE: To investigate the molluscicidal activities of the ginkgolic acid(GA) monomers isolated and purified from GAs. METHODS: Five monomers of GAs from the sarcotesta of Ginkgo biloba. were extracted by petrol ether, separated by silica gel column chromatography, purified by semi-prepared reversed-phased HPLC, and identified by LC-MS analysis. The molluscicidal activities of GAs and their monomers against Oncomelania hupensis were determined as referring to the WHO guidelines for laboratory molluscicidal test. RESULTS: The five purified ginkgolic acid monomers were GA(13:0), GA(15:0), GA(15:1), GA(17:1) and GA(17:2), with a side chain of 13, 15, 17 alkyl or ethylenic radicals res pectively on their benzene loop. The five monomer proportions to the total GAs were 17.6%, 3.2%, 52.3%, 23.3% and 3.6% respectively. The order of molluscicidal activities for the five monomers was as follows: GA(13:0)>GA(15:1)>GA(15:0)>GA(17:1)>GA(17:2), and their LC50 for snails was 20.79 mg/L, 22.28 mg/L, 33.76 mg/L, 51.89 mg/L, and 59.10 mg/L respectively after immersion for 24 hours. Two monomers, GA(13:0), and GA(15:1) inhibited the snails' climbing up significantly. CONCLUSION: The molluscicidal activities of GAs may be dependent on the monomer's structure with different number of carbon molecules and double-bonds on the side carbon-chain. The two monomers, GA(13:0) and GA(15:1), are mainly responsible for the molluscicidal activities of GAs and both effectively inhibit snails' climbing up as well. GA(15:0) also shows certain molluscicidal activity.