The authors experienced two cases of hydrochlorothiazide (HCTZ)-induced acute-onset bilateral myopia and shallowing of the anterior chambers. Two middle-aged women taking HCTZ, a sulfa derivative, visited our clinic complaining of acute bilateral visual deterioration. Both had good visual acuity without corrective lenses before taking HCTZ. A complete ophthalmologic examination revealed bilateral myopic shift, intraocular pressure elevation, shallowing of the anterior chambers, choroidal effusions, radiating retinal folds, and conjunctival chemosis. Approximately one week after HCTZ discontinuance, all ocular changes disappeared completely. Physicians should be aware of the adverse ocular effects of HCTZ and should manage patients accordingly.
Acute Disease ; Adult ; Anterior Chamber/drug effects ; Choroid/drug effects/*metabolism ; Cilia/drug effects/*metabolism ; Diuretics/*adverse effects ; Exudates and Transudates/*metabolism ; Female ; Humans ; Hydrochlorothiazide/*adverse effects ; Intraocular Pressure/drug effects ; Middle Aged ; Myopia/*chemically induced

OBJECTIVETo investigate the effects of lead exposure on the copper concentration in the brain and serum and the expression of copper transporters in the choroid plexus among rats.

METHODSSixty specific pathogen-free Sprague-Dawley rats were randomly divided into a control group and three lead-exposed groups, with 8 mice in each group. The lead-exposed groups were orally administrated with 500 (low-dose group)), 1 000 (middle-dose group), and 2 000 mg/L (high-dose group) lead acetate in drinking water for eight weeks. And the rats in control group were given 2 000 mg/L sodium acetate in drinking water. The content of lead and copper in the serum, hippocampus, cortex, choroid plexus, bones, and cerebrospinal fluid (CSF) was determined by inductively coupled plasma-mass spectrometry (ICP-MS). Confocal and real-time PCR methods were applied to measure the expression of copper transporters including copper transporter 1 (Ctr1), antioxidant protein 1 (ATX1), and Cu ATPase (ATP7A).

RESULTSCompared with the control group, the lead-exposed groups showed significantly higher lead concentrations in the serum, cortex, hippocampus, choroid plexus, CSF, and bones (P < 0.05) and significantly higher copper concentrations in the CSF, choroid plexus, serum, and hippocampus (P < 0.05). Confocal images showed that Ctr1 protein was expressed in the cytoplasm and cell membrane of choroid plexus in control group. However, Ctr1 migrated to CSF surface microvilli after lead exposure. Ctr1 fluorescence intensity gradually increased with increasing dose of lead, except that the middle-dose group had a higher Ctr1 fluorescence intensity than the high-dose group. In addition, the middle- and high-dose groups showed a lower ATX1 fluorescence intensity compared with the control group. Real-time PCR data indicated that the three lead-exposed groups showed significantly higher mRNA levels of Ctr1 and ATP7A compared with the control group (P < 0.05).

CONCLUSIONCopper homeostasis in the choroid plexus is affected by lead exposure to induce copper homeostasis disorders in brain tissue, which may be one of the mechanisms of lead neurotoxicity.

Adenosine Triphosphatases ; Animals ; Brain ; Cation Transport Proteins ; drug effects ; Choroid Plexus ; drug effects ; metabolism ; Copper ; metabolism ; Homeostasis ; Organometallic Compounds ; toxicity ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effects of acrylamide on the permeability of blood cerebrospinal fluid barrier (BCB) and tight junction protein ZO-1 of choroid plexus in rats and to provide a theoretical basis for explaining the mechanism of nerve injury induced by acrylamide.

METHODSThirty two male Sprague-Dawley rats were randomly divided into ACR and control groups. ACR group was exposed to 20 mg/kg ACR daily for 5 days a week by intraperitoneal injection (i.p.) for 4 weeks. Control group was exposed to normal saline. The neurobehavioral tests (including sensatory and motor functions) were performed every week. At the end of exposure, Evan blue (EB) and Sodium fluorescein (NaFI) content in rat CSF were detected for determining the BCB permeability, Real-time PCR was used to measure the expression levels of ZO-1 mRNA in the epithelium cells of choroid plexus, and laser scanning confocal microscope (LSCM) was utilized to observe the distribution of ZO-1 protein.

RESULTSNeurobehavioral tests showed that the tail-flick latencies of ACR group were 27.77% and 53.71% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). The hind lamb splay distances of ACR group were 131.76% and 153.77% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). Evan blue (EB) and Sodium fluorescein (NaFI) content of ACR group were significantly higher than those of control group (P < 0.05). In the 4th week, the expression level of ZO-1 mRNA in ACR group was 0.21 +/- 0.07, which was significantly lower than that (0.31 +/- 0.11) in control group (P < 0.05). In the 4th week, the ZO-1 protein expression level of choroid plexus in ACR group was significantly lower than that in control group (P < 0.05).

CONCLUSIONAcrylamide could increased the BCB permeability of rats, which may be involved in the central nervous injury induced by ACR.

Acrylamide ; toxicity ; Animals ; Blood-Brain Barrier ; drug effects ; Choroid Plexus ; metabolism ; Male ; Permeability ; drug effects ; Rats ; Rats, Sprague-Dawley ; Zonula Occludens-1 Protein ; metabolism