Nutritional and Environmental Influences on the Eye

Allen Taylor, Allen Taylor

• Publisher: CRC Press
• Year: 2021
• ISBN:
  9781000447712
• Edition: 1
• Topic: Medicine
• Subtopic: Biotechnology in Medicine

Significant advancements in nutrition's impact on the eye have occurred faster than any volume can document... until now. This book gives the background and rationale regarding the physiological damage caused by biological oxidants as well as the rationale for the protective roles for nutrient-antioxidants and how they affect the risk for cataracts.
This volume also contains information on how to quantitatively assess age-related diseases of the eye including cataracts and age-related maculopathy. Smoking and light exposure as factors for age-related eye diseases as well as the utility of potential anticataract pharmaceuticals is discussed.

Chapter 1 LENS AND RETINA FUNCTION: INTRODUCTION AND CHALLENGE

Allen Taylor

Vision is one of the most valued senses. Proper vision is achieved by a series of eye tissues working in concert. In simplistic phenomenological terms, light is collected in the anterior portion of the eye by the cornea and lens. It passes to the posterior of the eye where, in the retina, the light energy is transduced first to biochemical signals and then converted to electrical impulses before being passed on to the brain. Since most eye debilities involve dysfunction in the lens or retina, this book focuses on studies which elucidate the etiologies of debilities which affect these organs.

The lens is an elegantly simple tissue. It is made of only two types of cells: epithelial cells, which have not yet completely differentiated and not yet elaborated the major gene products, and fiber cells, in which these processes have been initiated or even completed (see Fig. 2, Chapter 4). Like red blood cells, the lens synthesizes a restricted group of major gene products, called crystallins. The crystallins fill the fiber cells, and proper packing of the fiber cells and the molecules within the fibers results in a clear lens.

The retina is the thin, transparent, light-sensitive neural tissue that originates from central nervous system tissue during embryonic development (see Fig.l, Chapter 11). The macula is a structure near the center of the retina that contains the fovea. This specialized portion of the retina is responsible for the high-resolution vision that permits activities such as reading. This tissue contains photoreceptor cells (both rods and cones) and neurons that convert the light images into electrical signals. The retina depends on cells of the adjacent retinal pigment epithelium (RPE) for support of its metabolic functions. Surrounding these organs and within them there are many other biological and molecular players.

In order to perform its function, the lens must remain clear throughout life. Various insults, including photooxidation, result in alteration and crosslinking of the long-lived lens proteins. These eventually aggregate and precipitate out of the normally clear milieu. Such precipitates are involved in cataracts. From a functional perspective, cataract is an opacity of the eye’s normally clear lens that interferes with vision. Cataract may develop at any time during life, although it is most often associated with advancing age. In addition to aging, cataract may be a consequence of diabetes and other metabolic disorders, trauma, exposure to ionizing radiation, or it may be inherited or congenital in nature.

The other major age-related lens problem, presbyopia, is the loss of the ability of the lens to focus from distant to near (known as accommodation), and involves rigidification of the lens. From a chemical and structural perspective, the modifications to lens proteins which result in cross-linking and thus, rigidification, are probably similar to changes involved in cataractogenenesis.

Photoreceptors in the retina, perhaps because of their huge energy requirements and highly differentiated state, are sensitive to a variety of genetic and environmental insults, many of which involve photooxidative stress. Thus, whereas the lens is avascular and the retina is highly vascularized and much more complex than the lens, the etiologies of these diseases may have much more in common than was previously thought.

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The loss of central vision in macular degeneration (MD) is devastating. Degenerative changes to the macula (maculopathy) can occur at almost any time in life but are much more prevalent with advancing age. With growth in the aged population, age-related macular degeneration (AMD) will become a more prevalent cause of blindness than both diabetic retinopathy and glaucoma combined.

The inspiration for putting together this book was my conviction that we are on the verge of achieving a means to diminish the risk for cataract and AMD. In order to foster this process, I chose to focus attention on research areas that are required in order to achieve a delay in onset or progress of cataract or AMD. As a prerequisite it is important to devise uniform means to evaluate eye tissue change. This will allow more comparison of various studies than is currently possible. Thus, the sum will be greater than its parts. It is also hoped that this summary will be a harbinger of and inspiration for research to follow, research that will expand our understanding of lens and retinal dysfunction, and which will allow further progress in diminishing risk for onset and progress of these debilities. Diminishing risk for onset of these debilities is of obvious benefit. Diminishing risk for progress of these debilities will allow, for the first time, treatment for those persons with incipient disease.

Consideration of the problem on a personal level and from a public health perspective offers a compelling justification for this research. Worldwide, 50 percent of all blindness is due to cataract. Although cataract treatment in this country is one of the most successful procedures, the only treatment involves surgical removal of the natural lens and replacement with a plastic implant. Each year an estimated $3.4 billion is spent through the Medicare program alone on the ≈ 1.4 million procedures which are performed each year. It is estimated that there were almost 34 million Americans over the age of 65 in 1995, and, by the year 2030, this number will more than double, and medical costs due to cataract and AMD can be expected to consume an ever-increasing proportion of the Medicare budget. Clearly there would be major fiscal and personal benefits if a means to delay onset or progress of cataract or AMD could be achieved.

There have been several summaries of previous information about lens and retina function. These studies have been augmented by recent advances in methods to observe and document lens and retina function and composition, as well as by a myriad of laboratory investigations which provide more information regarding normal function of these tissues.

Many of the ideas presented in this book are based on contemporary studies and may be accordingly biased. For example, it is currently widely believed that dysfunction of the lens is due to age-related alterations to many lens molecules. Whereas the lens, when considered in its entirety, is probably one of the slowest metabolizing tissues and the retina is probably one of the fastest metabolizing tissues, these tissues are found within millimeters of each other. Evolving data indicate that the age-related alterations in the retina have common features with those described for the lens. The most common alteration is oxidative change. This is caused by the high-energy forms of oxygen or other oxidants (i.e., peroxynitrite) as well as the light to which the eye tissues are exposed. Proteins, lipids and carbohydrates all undergo oxidative changes. These changes beget further modification and result in dysfunction on the molecular level. Such changes may be compounded since the molecules which are responsible for repairing or removing damaged molecules may themselves also be damaged. Thus the aging eye is in multiple jeopardy. Both the original constituents are damaged and the repair machinery is also compromised in function. It should be noted that, whereas the phenomena are common to both tissues, the damaging moieties may not be identical.

Nutrients provide potent antioxidative influence and may be exploited to delay damage to these tissues. Eventually, pharmacological agents may also be designed to provide protection against the age-related stresses which these tissues must endure.

The book is roughly divided into two portions. The first portion emphasizes studies regarding the lens and the second gives more attention to the retina. However, since many phenomena which apply to one tissue also are relevant to the other, no clear delineation is intended and considerable effort was made to crossreference the materials presented in each part of the text.

In order to present a contemporary overview of the field, the book starts in Chapter 2 with a theoretical explanation of oxidation and oxidative damage. This is followed in Chapter 3 by a description of the most modem means for evaluating lens opacity and changes in color. In Chapter 4 a summary is presented of many studies which describe age-related changes to the lens and the effects of nutrients on such changes in cell-free, in vitro, and whole animals. The chapter ends with a graphical summary of the clinical/epidemiological studies which seek to establish relationships between nutrition and risk for cataract in humans. Risk, in general, is given the most consideration, but risk for onset and progress of cataract is also discussed where possible. Various types of clinical studies are considered in this chapter. Accordingly, this chapter is followed in Chapter 5 by an evaluation of the value of various types of clinical studies. Most of the human studies had precedents in animal investigations, and these are documented briefly in Chapter 6. The advent of pharmacologicals to delay cataract onset or progress is on the horizon, and the means to evaluate such compounds and the results of some tests are summarized in Chapter 7.

In Chapters 8 and 9 the effects on age-related eye disease of light and smoking, respectively, are evaluated.

The focus of the text changes to the retina in Chapter 10. In this chapter various means to quantify retinal change are evaluated. This chapter is followed by a discussion of the etiology of age-related maculopathy and a summary of the clinical/epidemiological data regarding relationships between nutrition and risk for age-related maculopathy. Chapter 12 discusses the retinal carotenoids. New techniques are being developed to examine retinal constituents non-invasively, in vivo, in humans. A description of these very exciting developments concludes the book.

Chapter 2 OXYGEN RADICALS IN THE PATHOGENESIS OF CATARACTS–POSSIBILITIES FOR THERAPEUTIC INTERVENTION

Shambhu D. Varma, Ph.D., Palaniyandi S. Devamanoharan, Ph.D., and Ali H. Ali, B.Sc.

I. INTRODUCTION

Cataract is one of the major causes of visual impairment leading eventually to blindness. Fortunately, surgical removal of the cataract is successful in restoring adequate vision in most of the cases. However, the magnitude of the problem is so large that performing the surgery presents a significant public health burden. In the U.S.A. alone 1.35 million cataract extractions are performed every year. The problem is even much greater in the developing countries. Hence, studies on the pathogenesis of cataract and on development of pharmacological strategies to prevent its development have been very actively pursued over the last four decades....