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      Possible Mechanism of Exacerbating Cataract Formation in Cataractous Human Lens Capsules Induced by Systemic Hypertension or Glaucoma

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          To clarify the role of the lens capsule in cataract formation, changes in the protein conformational structure of immature cataractous lens capsules from patients with systemic hypertension or glaucoma have been investigated, as compared to normal lens capsules. The protein secondary structure and composition of these capsular samples were determined using Fourier transform infrared microspectroscopy with second-derivative, deconvolution and curve-fitting methods. We found that the composition of both random coil and β-type (β-sheet and β-turn) structures in the immature cataractous human lens capsules was increasingly induced by systemic hypertension or glaucoma, but α-helix content clearly decreased, leading to the alteration of protein conformational structures in lens capsules. A possible pathway of cataract formation exacerbated by systemic hypertension or glaucoma is discussed. According to the results, we propose that systemic hypertension or glaucoma induce changes in the protein conformational structures of the lens capsule, then cause alteration of membrane transport and permeability for ions, and finally increase intraocular pressure, resulting in the exacerbation of cataract formation. The effect on the conformational structure of cataractous human lens capsules is more pronounced for systemic hypertension than for glaucoma. The present study implies that systemic hypertension or glaucoma can exacerbate cataract formation in senile patients by modifying the protein secondary structures in the lens capsule.

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          Author and article information

          Ophthalmic Res
          Ophthalmic Research
          S. Karger AG
          11 December 2009
          : 29
          : 2
          : 83-90
          Departments of aOphthalmology and bMedical Research and Education, Veterans General Hospital Taipei and cNational Yang-Ming University, Taipei, Taiwan, Republic of China
          268001 Ophthalmic Res 1997;29:83–90
          © 1997 S. Karger AG, Basel

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          Pages: 8
          Original Paper


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