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1.
Int J Radiat Biol ; 95(7): 1043-1049, 2019 07.
Article in English | MEDLINE | ID: mdl-31157572

ABSTRACT

In the 60 years since the inaugural edition of the International Journal of Radiation Biology, much of our understanding of the biological effects of solar radiation has changed. Earlier in the century, sunlight played a 'hero's' role in reducing disabling rickets, while today debate still continues on the amount of sun required before exposure reveals the 'villainous' side of solar radiation. Although knowledge of the ultra violet (UV) component of sunlight as a carcinogen has become widespread, skin cancer rates are still rising yearly. Twentieth century attitudes have seen an about-face in the field of dermatological sun protection, with sunscreens changing from recipes designed to promote a 'healthy tan' to formulations proven to block both ultraviolet B (UVB) and more recently, ultraviolet A (UVA), to minimize premature sun-aging and skin cancer risk. In the early 1960s, DNA was first found to exist within mitochondria, while recently the connections between mitochondrial changes and UV radiation exposure have been expanded. Sixty years ago, understanding of the endocrine systems of mammals was enjoying its infancy. Early discoveries that light, particularly natural light, could have profound effects on functions such as sleep patterns and hormonal balance were made, while today more advanced knowledge has led to lighting improvements having pronounced effects on human wellbeing. Photosensitization 60 years ago was a health concern for both humans and their domestic animals, while today chemically engineered photosensitizing drugs can be administered along with highly directed light to pinpoint delivery targets for drug action. Life on earth is inextricably bound up with solar radiation. This article attempts to outline many of the ways in which our opinions about solar radiation have changed since the journal's inception.


Subject(s)
Radiobiology/history , Sunlight , Ultraviolet Rays , Animals , DNA/radiation effects , DNA Damage , DNA, Mitochondrial/metabolism , History, 20th Century , History, 21st Century , Humans , Mental Health , Mitochondria/radiation effects , Neoplasms/etiology , Neoplasms/radiotherapy , Photosensitizing Agents , Rickets/radiotherapy , Skin/radiation effects , Skin Aging/radiation effects , Skin Neoplasms/etiology , Skin Neoplasms/radiotherapy , Vitamin D/metabolism
2.
J Clin Invest ; 116(8): 2062-72, 2006 Aug.
Article in English | MEDLINE | ID: mdl-16886050

ABSTRACT

The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.


Subject(s)
Rickets/epidemiology , Vitamin D Deficiency/epidemiology , Calcium/metabolism , Child , Child, Preschool , Dihydroxycholecalciferols/metabolism , Female , Humans , Hydroxycholecalciferols/metabolism , Male , Phosphorus/metabolism , Prevalence , Rickets/etiology , Rickets/genetics , Rickets/radiotherapy , Ultraviolet Rays , Vitamin D/radiation effects , Vitamin D Deficiency/radiotherapy
3.
J Pediatr ; 123(2): 269-72, 1993 Aug.
Article in English | MEDLINE | ID: mdl-8345425

ABSTRACT

We describe a 15-year-old boy with hemangiomatosis of bone and hypophosphatemic rickets. The rickets was ameliorated by irradiation of the skeletal lesions.


Subject(s)
Bone Neoplasms/radiotherapy , Hemangioma/radiotherapy , Rickets/radiotherapy , Tibia , Adolescent , Bone Neoplasms/complications , Bone Neoplasms/pathology , Hemangioma/complications , Hemangioma/pathology , Humans , Male , Remission Induction , Rickets/complications
4.
Arch Dis Child ; 64(4): 617-9, 1989 Apr.
Article in English | MEDLINE | ID: mdl-2546510

ABSTRACT

An infant with chronic cytomegalovirus hepatitis and a child with atypical Alagille's syndrome had vitamin D deficiency rickets due to malabsorption. Both received ultraviolet irradiation. This treatment corrected biochemical abnormalities and healed the rickets. In the infant use of a sunlamp at home maintained normal 25 hydroxy-vitamin D for over a year. Our study shows that ultraviolet irradiation is an effective treatment of hepatobiliary rickets.


Subject(s)
Hepatitis/complications , Rickets/radiotherapy , Ultraviolet Therapy , Child , Cytomegalovirus Infections/complications , Female , Hepatitis, Viral, Human/complications , Humans , Infant , Male , Rickets/etiology
5.
J Invest Dermatol ; 77(1): 51-8, 1981 Jul.
Article in English | MEDLINE | ID: mdl-6265564

ABSTRACT

The skin has been recognized as the site for the sun-mediated photosynthesis of vitamin D3; until recently, however, very little was known about either the sequence of events leading to the formation of vitamin D3 in human skin or the factors that regulate the synthesis of this hormone. It is now established that, during exposure to sunlight, the cutaneous reservoir of 7-dehydrocholesterol (principally in the stratum Malpighii) converts to previtamin D3. Once this thermally labile previtamin is formed, it undergoes a temperature-dependent isomerization to vitamin D3 over a period of 3 days. The plasma vitamin-D binding protein preferentially translocates vitamin D3 from the skin into the circulation. During prolonged exposure to the sun, the accumulation of previtamin D3 is limited to about 10 to 15% of the original 7-dehydrocholesterol content because the previtamin photoisomerizes to 2 biologically inert photoproducts, lumisterol3 and tachysterol3. Increases in either latitude or the melanin concentration in the skin diminish the epidermal synthesis of previtamin D3. A single total body exposure to 3 minimal erythemal doses of ultraviolet radiation increased the vitamin-D3 levels in the serum 25-hydroxyvitamin-D levels after 7 days. The unique mechanism for the cutaneous synthesis, storage, and steady release of vitamin D3 into the circulation prompted an investigation into the potential therapeutic benefits of using the skin as the site for the synthesis and absorption of vitamin-D3 metabolites.


Subject(s)
Cholecalciferol/biosynthesis , Photosynthesis , Skin/metabolism , Animals , Cholecalciferol/blood , Cholecalciferol/metabolism , Humans , Rats , Rickets/radiotherapy , Skin/radiation effects , Skin Pigmentation , Sunlight
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