Characterization of Inhibitory Capability on Hyperpolarization-Activated Cation Current Caused by Lutein (ß,ε-Carotene-3,3'-Diol), a Dietary Xanthophyll Carotenoid.

Lutein (ß,ε-carotene-3,3'-diol), a xanthophyll carotenoid, is found in high concentrations in the macula of the human retina. It has been recognized to exert potential effectiveness in antioxidative and anti-inflammatory properties. However, whether and how its modifications on varying types of plasmalemmal ionic currents occur in electrically excitable cells remain incompletely answered. The current hypothesis is that lutein produces any direct adjustments on ionic currents (e.g., hyperpolarization-activated cation current, Ih [or funny current, If]). In the present study, GH3-cell exposure to lutein resulted in a time-, state- and concentration-dependent reduction in Ih amplitude with an IC50 value of 4.1 µM. There was a hyperpolarizing shift along the voltage axis in the steady-state activation curve of Ih in the presence of this compound, despite being void of changes in the gating charge of the curve. Under continued exposure to lutein (3 µM), further addition of oxaliplatin (10 µM) or ivabradine (3 µM) could be effective at either reversing or further decreasing lutein-induced suppression of hyperpolarization-evoked Ih, respectively. The voltage-dependent anti-clockwise hysteresis of Ih responding to long-lasting inverted isosceles-triangular ramp concentration-dependently became diminished by adding this compound. However, the addition of 10 µM lutein caused a mild but significant suppression in the amplitude of erg-mediated or A-type K+ currents. Under current-clamp potential recordings, the sag potential evoked by long-lasting hyperpolarizing current stimulus was reduced under cell exposure to lutein. Altogether, findings from the current observations enabled us to reflect that during cell exposure to lutein used at pharmacologically achievable concentrations, lutein-perturbed inhibition of Ih would be an ionic mechanism underlying its changes in membrane excitability.

Abnormal electroretinogram and abnormal electrooculogram after lightning-induced ocular injury.

PURPOSE: To report a case of abnormal electrooculogram and abnormal electroretinogram after lightning-induced ocular injury. DESIGN: Interventional case report. METHODS: A 39-year-old man was struck on the left forehead by a bolt of lightning. After resuscitation, he regained consciousness. RESULTS: Ophthalmic examination disclosed a best-corrected visual acuity of right eye (RE): 20/25 and left eye (LE): 20/50, burned eyelashes, punctate keratitis, iridocyclitis, anterior subcapsular lens opacity, missing foveolar reflex, and macular pigment epithelial defect LE. Fluorescein angiography revealed only an area of punctate leaking in the left eye. Electrooculogram showed reduced amplitudes, in the left eye. Arden ratio was RE: 2.04 and LE: 1.52. The amplitudes of scotopic and photopic electroretinogram b-waves were reduced in the left eye. After uneventful cataract surgery in the left eye, the follow-up electrooculogram and electroretinogram still showed reduced amplitude in the left eye. CONCLUSION: Lightning is an uncommon cause of ocular injury. This is the first report of abnormal electro-oculogram and abnormal electroretinogram after lightning-induced ocular injury.

Myopexy of the vertical rectus muscles using expanded polytetrafluoroethylene for management of a lost medial rectus muscle.

Strabismus due to a lost rectus muscle is uncommon. Surgical treatment of the condition by means of scleral augmented myopexy of the vertical rectus muscles can reduce the potential for anterior segment ischemia by leaving the vascular supply intact. We report a successful use of expanded polytetrafluoroethylene in this procedure to correct long-term exotropia caused by a lost medial rectus muscle.