Effects of ultraviolet light on the activity of an avian limb positional signalling region

Development ◽  
1982 ◽  
Vol 71 (1) ◽  
pp. 223-232
Author(s):  
Lawrence S. Honig

Cells from a region on the posterior margin of the developing avian limb bud (the polarizing region) can signal positional information to responding anterior cells. Polarizing activity may be assayed by disaggregation of the tissue into single cells, followed by reaggregation and grafting of cell pellet. This method enables treatments of the cells while in single-cell suspension. The effects of ultraviolet radiation (254 nm) were studied to determine the role of nucleic acids in polarizing activity. Ultraviolet radiation eliminated quail polarizing activity over the same range of doses as it reduced cell spreading (20–60 J/m2). In contrast to the published effects of γ-radiation in which polarizing activity is affected only at doses much higher than those that are cell lethal, ultraviolet apparently abolishes cell survival and polarizing activity at comparable doses. Compared to other biological systems, polarizing activity is quite sensitive to ultraviolet light: the D37 is 18 J/m2; the extrapolation number, n, is 3·6. From pomparison of the effects of ultraviolet radiation to those published for ionizing X- or γ-radiation, one may conclude that ultraviolet and γ-radiation abolish limb polarizing activity at equivalent nucleic acid dosages, not at equivalent cell lethal doses.


Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1700
Author(s):  
Melissa Chalada ◽  
Charmaine A. Ramlogan-Steel ◽  
Bijay P. Dhungel ◽  
Christopher J. Layton ◽  
Jason C. Steel

Uveal melanoma (UM) is currently classified by the World Health Organisation as a melanoma caused by risk factors other than cumulative solar damage. However, factors relating to ultraviolet radiation (UVR) susceptibility such as light-coloured skin and eyes, propensity to burn, and proximity to the equator, frequently correlate with higher risk of UM. These risk factors echo those of the far more common cutaneous melanoma (CM), which is widely accepted to be caused by excessive UVR exposure, suggesting a role of UVR in the development and progression of a proportion of UM. Indeed, this could mean that countries, such as Australia, with high UVR exposure and the highest incidences of CM would represent a similarly high incidence of UM if UVR exposure is truly involved. Most cases of UM lack the typical genetic mutations that are related to UVR damage, although recent evidence in a small minority of cases has shown otherwise. This review therefore reassesses statistical, environmental, anatomical, and physiological evidence for and against the role of UVR in the aetiology of UM.



2019 ◽  
Vol 105 (3) ◽  
pp. 839-853
Author(s):  
Aglaia Kyrilli ◽  
David Gacquer ◽  
Vincent Detours ◽  
Anne Lefort ◽  
Frédéric Libert ◽  
...  

Abstract Background The early molecular events in human thyrocytes after 131I exposure have not yet been unravelled. Therefore, we investigated the role of TSH in the 131I-induced DNA damage response and gene expression in primary cultured human thyrocytes. Methods Following exposure of thyrocytes, in the presence or absence of TSH, to 131I (β radiation), γ radiation (3 Gy), and hydrogen peroxide (H2O2), we assessed DNA damage, proliferation, and cell-cycle status. We conducted RNA sequencing to profile gene expression after each type of exposure and evaluated the influence of TSH on each transcriptomic response. Results Overall, the thyrocyte responses following exposure to β or γ radiation and to H2O2 were similar. However, TSH increased 131I-induced DNA damage, an effect partially diminished after iodide uptake inhibition. Specifically, TSH increased the number of DNA double-strand breaks in nonexposed thyrocytes and thus predisposed them to greater damage following 131I exposure. This effect most likely occurred via Gα q cascade and a rise in intracellular reactive oxygen species (ROS) levels. β and γ radiation prolonged thyroid cell-cycle arrest to a similar extent without sign of apoptosis. The gene expression profiles of thyrocytes exposed to β/γ radiation or H2O2 were overlapping. Modulations in genes involved in inflammatory response, apoptosis, and proliferation were observed. TSH increased the number and intensity of modulation of differentially expressed genes after 131I exposure. Conclusions TSH specifically increased 131I-induced DNA damage probably via a rise in ROS levels and produced a more prominent transcriptomic response after exposure to 131I.





Teratology ◽  
2002 ◽  
Vol 66 (6) ◽  
pp. 288-299 ◽  
Author(s):  
Chunwei Huang ◽  
Barbara F. Hales
Keyword(s):  


Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 326
Author(s):  
Magdalena Ciążyńska ◽  
Irmina Olejniczak-Staruch ◽  
Dorota Sobolewska-Sztychny ◽  
Joanna Narbutt ◽  
Małgorzata Skibińska ◽  
...  

The process of skin carcinogenesis is still not fully understood. Both experimental and epidemiological evidence indicate that chronic inflammation is one of the hallmarks of microenvironmental-agent-mediated skin cancers and contributes to its development. Maintaining an inflammatory microenvironment is a condition leading to tumor formation. Multiple studies focus on the molecular pathways activating tumorigenesis by inflammation and indicate several biomarkers and factors that can improve diagnostic and prognostic processes in oncology and dermatology. Reactive oxygen species produced by ultraviolet radiation, oxidizers, or metabolic processes can damage cells and initiate pro-inflammatory cascades. Considering the potential role of inflammation in cancer development and metastasis, the identification of early mechanisms involved in carcinogenesis is crucial for clinical practice and scientific research. Moreover, it could lead to the progress of advanced skin cancer therapies. We focus on a comprehensive analysis of available evidence and on understanding how chronic inflammation and ultraviolet radiation can result in skin carcinogenesis. We present the inflammatory environment as complex molecular networks triggering tumorigenesis and constituting therapeutic targets.



Development ◽  
1981 ◽  
Vol 61 (1) ◽  
pp. 207-219
Author(s):  
Katrina J. Kirkwood ◽  
W. D. Billington

Mixed haemadsorption assays using antibody-coaled indicator sheep erythrocytes and mouse alloantisera revealed that major histocompatibility complex (H-2) antigens were expressed on cells of 24–72 h cultures of mid-gestation mouse embryonic skin, gut, lung, limb-bud and heart but not of embryonic gonad or kidney. The precise time of detection of H-2 antigen expression and the proportions of cells expressing these determinants depended on inbred strain, specific haplotype, tissue of origin and antiserum batch employed. In all tissues the proportion of cells expressing H-2 increased progressively from day 11–12 postcoitum onwards. The findings are discussed with respect to hypotheses concerning the possible role of major histocompatibility antigens in cellular recognition and interactions during embryogenesis.



1991 ◽  
pp. 201-209
Author(s):  
Antony R. Young ◽  
Christopher S. Potten ◽  
Caroline A. Chadwick ◽  
Gillian M. Murphy ◽  
A. Jeffrey Cohen




2003 ◽  
Vol 2 (6) ◽  
pp. 286-294 ◽  
Author(s):  
Myeong Jun Choi ◽  
Howard I. Maibach


2002 ◽  
pp. 219-229
Author(s):  
Rolfdieter Krause ◽  
Jeanette Dobberke ◽  
Malte Buehring ◽  
Werner Hopfenmueller ◽  
Heinrich Kaase ◽  
...  


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