Publisher Summary The classification of cell death can be based on morphological or biochemical criteria or on the circumstances of its occurrence. Currently, irreversible structural alteration provides the only unequivocal evidence of death; biochemical indicators of cell death that are universally applicable have to be precisely defined and studies of cell function or of reproductive capacity do not necessarily differentiate between death and dormant states from which recovery may be possible. It has also proved feasible to categorize most if not all dying cells into one or the other of two discrete and distinctive patterns of morphological change, which have, generally, been found to occur under disparate but individually characteristic circumstances. One of these patterns is the swelling proceeding to rupture of plasma and organelle membranes and dissolution of organized structure—termed “coagulative necrosis.” It results from injury by agents, such as toxins and ischemia, affects cells in groups rather than singly, and evokes exudative inflammation when it develops in vivo. The other morphological pattern is characterized by condensation of the cell with maintenance of organelle integrity and the formation of surface protuberances that separate as membrane-bounded globules; in tissues, these are phagocytosed and digested by resident cells, there being no associated inflammation.

Cell death : the significance of apoptosis

The Optics of Human Skin

Administration of hematoporphyrin derivative i.v. followed by local exposure to red light has resulted in complete or partial response in 111 of 113 cutaneous or s.c. malignant lesions. Tumors treated have included carcinomas of the breast, colon, prostate, squamous cell, basal cell, and endometrium; malignant melanoma; mycosis fungoides; chondrosarcoma; and angiosarcoma. No type has been found to be unresponsive. In several cases complete clearing of chest wall metastatis has been achieved in treated areas. Deep-seated and pigmented tumors required a higher dose of drug for effective treatment than did the more superficial and nonpigmented lesions. A high therapeutic ratio between tumor and skin response has been obtained by allowing at least 3 days between drug injection and exposure to the therapeutic light for 2,5-mg/kg doses and at least a 4-day interval for 5.0-mg/kg doses.

https://cancerres.aacrjournals.org/content/canres/38/8/2628.full.pdf

Photoradiation therapy for the treatment of malignant tumors

The BCL2 protooncogene encodes an inner mitochondrial membrane protein that blocks programmed cell death. BCL2 was isolated from the chromosomal breakpoint of follicular B-cell lymphoma. Transgenic mice that overexpress BCL2 display extended survival of resting B cells. In this study we use a monospecific anti-human BCL2 antibody to define the distribution of BCL2 protein within organized tissues. BCL2 is restricted within germinal centers to the follicular mantle and to portions of the light zone implicated in the selection and maintenance of plasma cells and memory B cells. BCL2 is present in the surviving T cells in the thymic medulla. All hematopoietic lineages that derive from a renewing stem cell also display BCL2. A limited number of nonlymphoid tissues demonstrate BCL2 and can be grouped as (i) glandular epithelium in which hormones or growth factors regulate hyperplasia and involution, (ii) complex differentiating epithelium such as skin and intestine characterized by long-lived stem cells, and (iii) long-lived postmitotic cells such as neurons. Within these tissues that demonstrate apoptotic cell turnover, BCL2 is often topographically restricted to long-lived or proliferating cell zones. BCL2's function as an antidote to apoptosis may confer longevity to progenitor and effector cells in these tissues.

https://www.pnas.org/content/pnas/88/16/6961.full.pdf

BCL2 protein is topographically restricted in tissues characterized by apoptotic cell death.

DNA is taken as the target for skin cancer induced by ultraviolet light, and the known data on the sensitivity of DNA as a function of wavelength are summarized. The sun's spectrum at the surface of the earth and the DNA action spectrum are used to calculate the carcinogenic effectiveness as a function of wavelength. The most effective wavelengths at 30°N latitude are <305 nm, and a 1% change in atmospheric ozone results in a 2% change in the effective dose of ultraviolet light. Since both the basic biological and physical data are reasonably precise, the major requirement for a quantitative evaluation of the dose response relation for ultraviolet-induced skin cancer in man is better epidemiological data to compare with data from animal models.

https://www.pnas.org/content/pnas/71/9/3363.full.pdf

The wavelengths in sunlight effective in producing skin cancer: a theoretical analysis.

— The u.v. transmission characteristics of various epidermal specimens prepared by various methods were measured by a recording spectrophotometer and integrating spheres. Although suction or stretch and heat produced the most satisfactory specimens, transmission data obtained from all specimens were similar and generally resembled that reported by previous investigators. The important contribution of forward scattering to total transmitted light was demonstrated. Significant numbers of u.v. photons have been shown to penetrate to the dermis and papillary capillaries. Erythema was produced in vivo by monochromatic light filtered through epidermal specimens after exposure of skin to the quantity of u.v. anticipated by these data.

Penetration of epidermis by ultraviolet rays.

SUMMARY.— Melanosomes are formed within melanocytes and transferred via dendrites to keratinocytes. In caucasoids, most melanosomes are aggregated in membrane-bound organelles (melanosome complexes). These aggregates have phagocytic capacity, stain positively with aryl sulphatase and acid phosphatase, contain melanosomes apparently undergoing degradation, and are lysosomes. In addition to melanosome complexes, individual melanosomes, both in melanocytes and keratinocytes, also exhibit lysosomal properties of phagocytosis and hydrolytic enzyme activity. In contrast, negro melanosomes are mostly singly dispersed and are rarely aggregated in complexes. Melanosome dispersal contributes to the darker colour and superior sunlight protection of negro skin. Degradation by lysosomal enzymes explains the limitation of melanin principally to the basal layer.

In skin with severe solar degeneration, particularly in xeroderma pigmentosum, pigment production is often apparently adequate since hypertrophic melanocytes and dendrites are conspicuous. However, pigment transfer from melanocytes to keratinocytes does not occur normally. Some keratinocytes contain little melanin while others show an increase. Melanosomes within keratinocytes of actinically damaged skin tend to be concentrated within larger than normal complexes. Skin colour and sunlight protection appear to depend not only upon the rate of melanin formation but also upon distribution and rate of degradation.

The role of epidermal lysosomes in melanin physiology.

Apoptosis is a process found in many tissues by which devitalized cells are eliminated in an orderly manner. In skin, apoptosis occurs following sunburn, in Bowen's disease and in basal cell carcinoma. Scattered cells are observed in which the cytoplasm has become condensed and dyskeratotic. These dyskeratotic cells are phagocytized, either in toto or in fragments by surrounding keratinocytes. This process involves the condensation, fragmentation, phagocytosis and digestion of individually degenerated cells. The mass of a tissue is thus related to the balance between cell formation (mitosis) and cell destruction (apoptosis). In epidermal and other surface tissues, the rate of exfoliation must also be considered.

Epidermal Apoptosis: Cell Deletion by Phagocytosis

Characteristic cells have been demonstrated as being individually dispersed throughout the superficial epidermis 24 h after being exposed to ultraviolet light. These „sunburn cells” with cosinophilic cytoplasm and pyknotic nuclei observed by light microscopy are also observed to be dyskeratotic by using electron microscopy.

Ultraviolet-induced individual cell keratinization.

—The epidermis of 6 patients with actinic degeneration was studied by electron microscopy. In comparison with nonexposed skin of the buttock, sections from exposed areas revealed abnormalities of 3 epidermal cellular functions. Epidermal cells were characterized by focal areas of dej^eneration involving groups of adjacent cells. Degenerative changes resembling dyskeratosis were present in cytoplasm of basal as well as spinous cells. Secondly, cellular cohesion was disturbed. Desmosomes varied from few to greatly increased in quantity, and exhibited variable degrees of maturity and distribution. The third disturbance was in epidermal pigment distribution. Melanin concentration varied from none to excessive, and melanosome complexes were often abnormally large. These clones of epidermal aberrations, visible by electron microscopy when no light microscopic or clinical abnormalities are present, suggest that epidermal alterations induced by u.v. light may parallel or even precede dermal damage.

Ultrastructure of human epidermis following chronic sun exposure.

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