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With the extensive use of plastic products and the sharp increase of plastic waste, microplastics produced by degradation in the natural environment and artificially added by industry have been detected in food, air, ocean, and even extreme geographical environment. The environmental pollution and the biological health hazards caused by this new type of pollutant has become a global scientific problem to be solved urgently. Zebrafish (Danio rerio), as a typical model organism, has been widely used to evaluate the environmental pollution and health hazards caused by microplastics. This review on the research progress of model animal zebrafish in toxicity evaluation of microplastics mainly emphasized the toxic effects of microplastics on selected organs of zebrafish, briefly introduced the influencing factors of toxicity induced by microplastics, discussed the standardization of experiments for the evaluation of microplastic toxicity using zebrafish, and finally explored the future research directions.
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AIM: To investigate the effect of flutamide on mitochondrial biogenesis and the regulating effect of anoxidative pathway Nrf2 on it. METHODS: Human hepatocyte HepG2 cells were treated with flutamide (0-50 μmol/L) for 24 h, then mtDNA copy number and protein expression of mitochondrial biogenesis were detected by RT-PCR and WB. The effects of ERK1/2 and the role of Nrf2 pathway in mitochondrial biogenesis were further observed by gene knockdown and protein activation/inhibition methods. RESULTS: Flutamide interfered mitochondrial biogenesis concentration-dependently, the mtDNA copy number, ERK1/2 and PGC-1α proteins increased with the dose. ERK1/2 inhibition and activation regulated flutamide-induced mtDNA copy number and PGC-1α expression, and inhibition of Nrf2 pathway also affected flutamide-induced mtDNA copy number and expression of PGC-1α, as well as ERK1/2 expression. CONCLUSION: Flutamide affects mitochondrial biogenesis, and the antioxidant pathway Nrf2 may be involved in the regulation of flutamine-induced mitochondrial biogenesis by regulating ERK1/2.
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BACKGROUND:Compared with the cone stem,short stem holds good matching with femoral canal,and remarkably reduces the risk of prosthesis loosening.OBJECTIVE:To further investigate the clinical efficacy of Accolade Ⅱ stem for Crowe type Ⅰ developmental dysplasia of the hip.METHODS:Clinical data of 16 patients with Crowe type Ⅰ developmental dysplasia of the hip undergoing total hip arthroplasty using Accolade Ⅱ stem were collected,the length of both lower limbs before and after surgery was compared,and the Visual Analogue Scale,functional recovery of the hip and general conditions were observed at 12 weeks postoperatively.RESULTS AND CONCLUSION:(1) The change in length of both lower limbs before and after surgery had significant difference (P ＜ 0.05),and 10 patients (62％) with the same length of both lower limbs before surgery,and 15 cases (94％) after surgery.(2) The postoperative acetablar abducent angle was 41°-54° (average 46.9°).(3) The Visual Analogue Scale and Harris hip scores after surgery were significantly improved compared with baseline (P ＜ 0.05).(4) The intraoperative blood loss was 147 mL on average,the mean operation time was 72 minutes,and the hospitalization time was 7.2 days.(5) All patients recovered well and no complications occurred at 3 months postoperatively.(6) To conclude,Accolade Ⅱ stem is safe and reliable for Crowe type Ⅰ developmental dysplasia of the hip,and exhibits good functional recovery of the hip.
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The purpose of risk assessment is to evaluate the permissible exposure level under specific risk factors.To extrapolate the human acceptable daily intake (ADI) and/or reference dose (RfD), the traditional method uses the no-observed-adverse-effect level ( NOAEL ) to quantify toxicity after being divided by uncertainty factor.There are many limitations with NOAEL method in safety evaluation,for it relies too much on experimental design.Benchmark dose ( BMD) approach is a more reliable method with many advantages.BMD approach and its analysis software, the advantages of BMD over NOAEL, the application and methodological perfection in risk assessment of long-team exposure toxicity are presented in this review.
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Metallothionein ( MT ) is a cysteine-rich and low-molecular metal binding protein. Three isoforms of MT have been found in the central nervous system, including MT-Ⅰ, Ⅱ, and Ⅲ. MT is widely involved in many critical activities in the central nervous system, such as neuronal growth, auto-defensive reaction, immune-regulation, and repair of cerebral injury. MT exerts many important biological functions like scavenging of free radicals, regulation of ion homeostasis in brain cells, detoxification of heavy metals, anti-inflammation, and anti-apoptosis. Recently, MT has been increasingly shown to have protective effects against cerebral ischemia. MT promises to be an important target for prevention and/or treatment of cerebral ischemic disease. ln this review, the expression and regulation characteristics, and the effect of cerebral ischemic stress on MT expression have been summarized, with focus on the neuro-protective effect of MT and its possible underlying mechanisms.
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AIM: To investigate the effects of metallothionein (MT) induced by zinc on doxorubicin (DOX)-treated mice and to explore the potential mechanisms. METHODS: Male C57BL/6J mice were divided randomly into 4 groups (n = 6) following control, DOX, Zn and Zn plus DOX. Mice were pretreated with eikg-1, ip) or equal volume of saline, and were killed on d 4 after the last injection. Serum and hearts were collected for examination. RESULTS: Zinc pretreatment elevated cardiac MT levels significantly while other antioxidants in heart including glutathione (GSH), glutathione peroxidase (GSHpx) , superoxide dismutase (SOD), and catalase (CAT) were not altered. Severe oxidative injury occurred in the mice treated with DOX as myocardial lipid peroxidation and morphological changes manifested by myocardial fibers swelling and vacuolization and nuclear condensation or dissolution, with increased activities of serum creatine kinase and lactate dehydrogenase and depletion of GSH, GSHpx, and SOD while CAT activity was increased in compensation. However, pre-induction of MT with zinc attenuated all of these toxic changes significantly. Furthermore, DOX induced elevation of hydrogen peroxide in heart tissues was greatly inhibited by zinc pretreatment. CONCLUSION: Preinduction of MT by zinc protects the heart from DOX-induced cardiotoxicity, and this effect is possibly correlated with the property of MT on scavenging free radicals in vivo.