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Lens (eye)
Focus in an eye.svg
Light from a single point of a distant object and light from a single point of a near object being brought to a focus by changing the curvature of the lens.
Latin lens crystallina
Gray's subject #226 1019
MeSH [1]
Schematic diagram of the human eye en.svg
Schematic diagram of the human eye.

The lens is a transparent, biconvex (lentil-shaped) structure in the eye that, along with the cornea, helps to refract light to be focused on the retina. Its function is thus similar to a human-made optical lens. The lens is also known as the aquula (Latin, a little stream, dim. of aqua, water) or crystalline lens.

In humans, the refractive power of the lens in its natural environment is approximately 15 dioptres, roughly one-fourth of the eye's total power.


The main function of the lens is to change the focal distance of the eye to allow focusing on objects at various distances. This adjustment of the lens is known as accommodation (see also Curvature and Thickness, below). It is similar to the focusing of a photographic camera via movement of its lenses. Adjustment of the lens is controlled by the nervous system and executed by a system of muscles around the lens to allow a sharp image of the object of interest to be formed and detected on by retina.


The average adult human lens is about 5 mm thick and has a diameter of about 9 mm. Its thickness can be adjusted by surrounding muscles, and crystallins are its main protein building blocks.

Curvature and thickness


An image that is partially in focus, but mostly out of focus in varying degrees.

The lens is flexible and its curvature is controlled by ciliary muscles through the zonules. By changing the curvature of the lens, one can focus the eye on objects at different distances from it. This process is called accommodation. At short focal distance the ciliary muscles contract, zonule fibers loosen, and the lens is thick resulting in a high refractive index. Changing focus to an object at a distance requires the stretching of the lens by the ciliary muscles which reduces the refractive index and increases the focal distance.

The lens continually grows throughout life, laying new cells over the old cells resulting in a stiffer lens. The lens gradually loses its accommodation ability as the individual ages, the loss of the individual's focusing ability is termed Presbyopia.

Composition: crystallins

The lens is mostly made of transparent proteins called crystallins at an average concentration of about twice that of other intracellular proteins. Crystallins are thought to be key to the refractive properties of the lens while at the same time allowing most light to pass through.

The proteins are arranged in approximately 20,000 thin concentric layers, with a refractive index (for visible wavelengths) varying from approximately 1.406 in the central layers down to 1.386 in less dense cortex of the lens[1]. This index gradient enhances the optical power of the lens. The lens is included into the capsular bag, maintained by the zonules of Zinn.


The lens forms from an inverted section of ectoderm. During the fetal stage, the development of the lens is aided by the hyaloid artery.


In adults, the lens depends entirely upon the aqueous and vitreous humors for nourishment.


  • A cataract is an opacification of the normally transparent crystalline lens that leads to blurred vision.
  • Ectopia lentis is a displacement or malposition of the lens from its normal location.
  • Nuclear sclerosis is a normal age-related change of the center of the lens; in veterinary medicine, most commonly seen in dogs.
  • Aphakia, the absence of the natural crystalline lens of the eye.
  • Presbyopia


The common disease diabetes affects the lens causing blurred vision. The underlying molecular cause is probably non-enzymatic addition of glucose (glycation) to lens proteins, mainly crystallins. This causes them to form aggregates that obstruct the passage of light through the lens [2].

The late diabetic symptom of blindness is probably due to effects on hyperglycemia (elevated blood glucose) on the retina not the lens (see diabetic retinopathy).

Additional images


  1. Hecht, Eugene. Optics, 2nd ed. (1987), Addison Wesley, ISBN 0-201-11609-X. p. 178.
  2. Perry RE, Swamy MS, Abraham EC (1987). Progressive changes in lens crystallin glycation and high-molecular-weight aggregate formation leading to cataract development in streptozotocin-diabetic rats. Exp. Eye Res. 44 (2): 269-82.

See also


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