24.11.2014
Black lights are not that different from any other type of light, whether incandescent, fluorescent, or just the age old candle flame. The construction of bulbs that create UV light is fairly simple, though there are several different ways to go about making “black lights”. A normal Fluorescent bulb creates light by channeling electricity through a conductive inert gas. So whether you want to throw a “Rave” and know for sure who’s been brushing their teeth, or check your hotel sheets for blood, urine, and semen, black light is a phenomenon that everyone seems to enjoy! UVB radiation was once thought to be the dominant precursor to skin cancers from UV radiation. Ever wonder how tanning booths can make you burn in 10 minutes while it may take hours in sunlight? Aside from revealing those around you who have dandruff, black lights have very practical purposes. Another ingenious use for black lights is to diagnose certain types of bacterial infections. Some common vitamins that fluoresce include A, and B vitamins, niacin, thiamine, and riboflavin. On average in the United States, UVB radiation is most prevalent between 10AM and 4PM from April to October.
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The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. The difference is that black lights emit most of their light waves just outside the range humans can perceive, in the Ultraviolet (UV) part of the spectrum.
When a photon from UV light hits the phosphorous material, it causes the electrons to get excited and stray farther from the nucleus than they normally would. Electromagnetism is one of the four fundamental forces in the universe, the others being gravity* and the nuclear weak and strong forces  This “light” radiation comes in many forms you probably recognize, from the long wavelength (low frequency radio waves, microwaves, and infrared waves), to the shorter wavelength (higher frequency ultraviolet waves, x-ray waves, and Gamma-ray waves).
They add a small amount of mercury inside the tube, or bulb, that will give off light photons when energized.
So shut off all the visible light sources and let the black light show you what you most likely never wanted to see! Tanning booths emit UVA light sometimes as much as 12 times that of what reaches us from the Sun. Some bacteria naturally fluoresce under UV light and, as such, certain infections can be diagnosed by shining a black light on the patient. Bacteria have proteins in their cell walls that will bind with water, even when the microbe itself is dead. These materials all tend to have rigid molecular structures that contain delocalized electrons (ones that are not associated with any specific atom within the molecule). This diagram illustrates the wavelengths of typical waves in different regions of the UV spectrum. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. When a UV light wave hits an object containing substances known as phosphors, those phosphors will naturally fluoresce, and glow. When the electron falls back to its normal state, some of the energy is lost in the form of heat.
Right in the middle of these is a sliver of the spectrum that we can see with our human eyes, namely visible light waves.
This is because UVA radiation is less intense and it penetrates more deeply than UVB; so it was thought that they did not damage the outermost layer of the skin (epidermis).
So the next time you feel like getting a tan via a tanning bed, know that people who use tanning booths are 2.5 times more likely to get squamous cell carcinoma and 1.5 times more likely to develop basal cell carcinoma, neither of which do you want to get! Most laundry detergents will also fluoresce, which helps your white clothes glow extra bright under a black light. I hope you don’t mind a little constructive criticism, because otherwise this is a well written and informative article.
Short wavelengths correspond to higher frequencies and higher energies, while longer waves oscillate at lower frequencies and carry less energy. The skin covers the whole body surface and acts as a dynamic barrier to prevent water evaporation from the human body. When the UV light wave is reflected back to your human eyes, it now has less energy, therefore a shorter wavelength. Instead of creating light in the visible spectrum, the coating absorbs harmful UV-B and UV-C light waves and creates UV-A waves.
All of the light that is created by the heated filament is filtered out, except those waves in the infrared and UV-A spectrum.  The filter absorbs the rest, which is why this type of black light tends to get extremely hot, even for an incandescent bulb, and has a short lifespan.
Numerous recent studies have disproved that theory and UVA waves have been shown to damage skin cells at the basal layer of the epidermis, which is where most skin cancers occur.
For you teenage girls out there who just love your booth time, you should know that the first session you get in a tanning bed will increase your risk of melanoma by 75%.
This type of bacteria has 191 known species and is the second leading cause of infections in hospitals.
Red and blue waves from the visible light portion of the electromagnetic spectrum are also shown for comparison. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. It also prevents the entrance of noxious substances and pathogens into vital internal organs [2].
To get the visible light out of the bulb, a phosphorus coating is applied to the glass and reacts to the UV waves and creates the visible light hospitals everywhere are famous for!
UVC wavelengths are absorbed by the ozone layer and as such do not reach us here on the Earth surface.
Yes, that’s just after the first exposure!  Save yourself a lot of potential medical grief and improve how your skin will age by skipping purposefully tanning altogether.  Better to be pale than prematurely wrinkly or, you know, dead from skin cancer.
When attracted to the source, they will receive a life-ending shock from whatever electrical mechanism that surrounds the light. Some ski resorts have caught on to this little phenomenon and have started adding dead microbes to their artificial snow-making machines. According to the Standard Model of Particle Physics, it is a currently accepted notion that gravity is indeed a fundamental force.
When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression.


A network composed of delicate physical, chemical, and immunological barriers in the skin makes it a perfect organ to protect the integrity of the human body [3].
The end result being, you cannot see the majority of the light coming from the source, but you can see its reflection off of objects containing phosphors. One of the reasons humans can see more of the light from a bug zapper, than from any other black light, is that bug zappers use clear glass (because it’s cheaper) instead of filter coated glass.
Scientists have also discovered that natural snow contains large amounts of these microbes.
As mentioned, there are several types of body fluids that will glow under UV light, blood, semen, and urine for example. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis.
However, the integrity of skin barriers can be impaired by exogenous factors, including ultraviolet rays (UVR). Though helpful for the ski resorts, one type, Pseudomonas syringae, is a nuisance for farmers as it almost immediately destroys crops and plants below freezing. Intriguingly, receptor activator of NF-?B (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. In this review we discuss the effect of UVR on human skin with a focus on physiological and pathological apoptosis. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Physiological apoptosis in the skin is reflected by the terminal differentiation of epidermal keratinocytes, which lose their nuclei when undergoing upward differentiation and manifest as gross scale shedding. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes.
Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. The pathological apoptosis, on the other hand, may lead to benign proliferative inflammatory disease (such as psoriasis vulgaris) and neoplastic growth. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases. We also review the application of UVR-based phototherapy in medical care focusing on apoptosis and its related biological effects in different skin residential cells. The Biological Relevance of UVR to SkinDepending on the wavelength, UVR (100–400 nm) can be divided into three parts—UVA (315–400 nm), UVB (280–315 nm), and UVC (100–280 nm) [10]. UVC has the shortest wavelength and the highest energy, although most of the solar UVC is blocked by the ozone layer. Thus, UVC is most harmful to genetic integrity, but it seldom reaches human skin due to its absorption by ozone layers. UVA has the longest wavelength with the lowest energy and can penetrate deeply into the dermis and cause aging effects [11]. UVB, which has a wavelength spectrum in between UVC and UVA, can cause redness of the skin and contribute to most of the UVR entering the dermis.
Since UVB is only partially blocked by clouds or fog, UVB radiation is considered as the main cause of sunburn and skin cancers [12]. In fact, both UVB and UVA radiation contribute to freckling, skin wrinkling and the development of skin cancers [13,14].
Since the skin is composed of different layers of varying depths with different physical and chemical properties, UVR exerts different biological effects on different kinds of cells in the skin (Figure 1). The p53 directly interacts with nucleotide excision repair (NER)-associated regulatory proteins. The mutations in the NER machinery can cause xeroderma pigmentosum (XP), an autosomal recessive disease with impaired DNA repair after UV radiation and early development of skin cancers [30].
Several studies have demonstrated that DNA repair is impaired in the absence of functional p53 [31].
Compared with the wild-type mice, knockout mice lacking the p53 protein show a reduction of sunburn cells in the epidermis following UVB irradiation [32]. Mutated p53 with defective function is commonly present in non-melanoma skin cancers and actinic keratosis, a premalignant lesion that may give rise to invasive squamous cell carcinoma [33]. On the other hand, basal keratinocytes also exhibit p53-independent apoptosis (described below) following UV radiation. However, upon induction of differentiation to committed progenitor cells, the apoptosis is dependent on p53-related signaling pathway. Although apoptosis is p53-independent in basal keratinocytes, DNA repair is p53-dependent in other cell types of skin tissues.
Thus, p53 acts as an important regulator of DNA repair but it is not involved in the apoptosis of basal keratinocytes. Intrinsic Pathways in UV-Induced ApoptosisThe intrinsic pathway involved in UVR-induced apoptosis results from DNA damage and cytochrome c release from mitochondria (Figure 2) [39,40]. Permeation of the mitochondrial outer membrane [39,40] and leakage of cytochrome c into the cytosol triggers a caspase cascade. Once released, cytochrome c and the apoptotic protease activating factor-1 (Apaf-1) together form the apoptosome, a protein complex that recruits and activates Caspase 9 [41].
The balance of pro-apoptotic (Bax, Bak and Bid) and anti-apoptotic (Bcl-2 and Bcl-x) members of the Bcl-2 protein family determine the initiation or the inhibition of apoptosis [39].
Bcl-2 inhibits Caspase 3 and Caspase 8 activation, while Bcl-x partially inhibits cytochrome c release [42].
One of our previous studies showed that, in primary keratinocytes, UVB induces keratinocyte apoptosis via suppression of Bcl-2 expression (intrinsic) and activation of Caspase 8 (extrinsic) [43]. A combined use of UVB irradiation and arsenic treatments has been found to result in the anti-proliferative and pro-apoptotic effects by activation of Caspase 8 and 9 in keratinocytes [44,45]. It also has been reported that p53 can interact with the mitochondria-mediated pathway and Bcl-2 and Bcl-xL proteins to regulate apoptosis [46,47].
On the other hand, the epidermis contains several antioxidant enzymes including superoxide dismutase, glutathione peroxidase and catalase, which can remove ROS from the skin [48] and are depleted by prolonged exposure to UV [49].
Free radical scavengers, such as vitamins C and E, carotenoids and glutathione are also localized on the skin to prevent the damaging effects of ROS [50]. It has been documented that large-scale deletions of mitochondrial DNA (mtDNA) are present in sun-exposed skin tissues [51,52]. In one of our previous studies, we showed that a high proportion of mtDNA deletion rendered human cells more susceptible to UV-induced apoptosis through enhanced release of cytochrome c [53]. We demonstrated that human skin fibroblasts harboring pathogenic mutations of mtDNA were more susceptible to apoptosis triggered by UV irradiation or oxidative stress.
This may provide a regulatory mechanism for the skin to exert quality control of mitochondria and to prevent further increase of oxidative damage or associated pathological changes under oxidative stress. Taken together, the results from the other investigators and our laboratory indicate that oxidative stress and damage elicited by mtDNA mutations not only lead to mitochondrial dysfunction but also increase the susceptibility of affected skin tissue cells to apoptosis upon UV irradiation [54–56].


UV Induces Melanogenesis and Apoptosis in Melanocytes Differentially Based on Wavelength and DosePhysiologically, UVR is known to induce synthesis of melanin in the melanocytes and melanin is important in the protection of harmful effects of UV (Figure 3) [75].
Several studies have reported that exposure of the skin to UV results in increased synthesis of paracrine factors, such as ACTH, endothelin-1, ?-FGF, and ?-MSH, which play an important role in mediating the UV response of human melanocytes [76]. For example, ?-MSH is known to reduce the generation of UV-induced DNA photoproducts by enhancing nucleotide excision repair (NER) and to diminish the induction of oxidative DNA injury through elimination of ROS [77,78]. In addition to the induction of paracrine factors, UV can induce the activation of the transcription factors USF-1, Mitf, ATF-2, Nrf-2 and p53, and inhibition of NF?B [76].
The dynamics of melanogenesis induced by repeated exposures depends on UV dose, dose interval and emission spectrum with UVA generally being stronger than UVB to induce pigmentations [79].
There is also evidence that increasing the UV dose above a certain level of cumulative exposure does not significantly increase the level of UV-induced pigmentation [80].
Similar to that seen in keratinocytes, UV induces cell cycle arrest, activation of antioxidant and DNA repair enzymes, and regulation of apoptotic pathways in melanocytes, to ensure genomic integrity and survival of melanocytes [76].
These regulatory processes enhance melanogenesis to confer appropriate photoprotection of the epidermis against UV-induced damage (Figure 3). Therefore, unraveling the mechanisms by which the stress response of melanocytes to UV and more specifically, the regulation of DNA repair pathways, in melanocytes might lead to strategies to prevent malignant melanoma, a rapidly-fatal malignancy derived from melanocytes [76].
Application of Phototherapy: UV-Induced Apoptosis and Biological ConsequencesThe first recorded UV therapy was performed by Dr.
Niels Finsen, the 1903 Nobel Laureate in Physiology or Medicine, who demonstrated that UV has a positive effect on lupus vulgaris, a form of skin tuberculosis [91]. Although few theories exist how Finsen UV therapy worked against lupus vulgaris, Wulf’s group thought that Finsen used UVA radiation and that it acted through photosensitization and ROS production by porphyrins in the bacteria [92].
The involvement of UV-induced apoptosis in this therapy is unclear, though photosensitization and oxidative injury may play a role.
Table 1 lists several clinical techniques related to the phototherapy widely applied in medicine.
Visible light in the blue-green range (430–490 nm) has been used as a standard treatment of neonatal jaundice, for example. The tissue bilirubin, possessing the heme group, absorbs the light in this spectrum and the metabolites become more lipophilic than the mother compound and are more readily excreted [92].
Although the mechanism is not related to apoptosis, the blue lamp has been shown to form more photo-oxidation products and cause more severe cellular damage and apoptosis in the presence of bilirubin as compared to the green lamp [93].Currently, irradiations with broadband UVB (290–320 nm), narrowband UVB (311–313 nm), 308 nm excimer laser, UVA 1 (340–400 nm), UVA with psoralen (PUVA), and extracorporeal photochemotherapy (photopheresis) are in use [105]. Electromagnetic waves (EMW) in different wave lengths have various effects in the skin that occur as a result of photoselective thermolysis, evaporation, immunosuppression, abnormal DNA repair, apoptosis, and melanogenesis in different types of skin residential cells. The different biological effects of those EMW therapies have been applied in treatment of several human diseases.
Clinically, several diseases are treated with UVB-based phototherapy, including psoriasis, atopic dermatitis, vitiligo, cutaneous T-cell lymphomas, and morphea [98] because UVB have an effect on cell proliferation, apoptosis, and immunomodulation.
Due to the development of modern UVB lamps that are easily applicable, UVB phototherapy is more often used than PUVA. However, even though UVB phototherapy is very efficient in the treatment of psoriasis, it is less frequently used by dermatologist than it was 10–20 years ago [106,107].
Narrowband UVB has increased efficacy in psoriasis treatment over broadband UVB and is safer than PUVA [108].UVA1 can be used to treat many diseases and has been shown scientifically to be effective in the treatment of localized scleroderma and atopic dermatitis. UVA1 induces cyclobutane pyrimidine dimers but not 6–4 photoproducts in human skin in vivo[109].
UVA1 exerts its therapeutic effects through T cell apoptosis, collagenase induction, angiogenesis, tissue remodeling [97]. Psoralen ultraviolet A (PUVA), on the other hand, is a form of chemophototherapy which utilizes UVA to activate psoralens, a photoreactive chemical [110]. When irradiated with UVA, psoralens can inhibit DNA replication and cause cell cycle arrest and ultimately apoptosis. Psoralen photosensitization also causes an alteration in the expression of cytokines and cytokine receptors [111].
Psoralens directly interact with RNA, proteins and other cellular components and indirectly modify them via ROS [112]. Epidermal and dermal infiltrating lymphocytes are robustly suppressed by PUVA, with varying effects on different T-cell subsets [113]. Like UVB, PUVA can also stimulate melanogenesis and inhibit immune responses [114].Photodynamic therapy (PDT) utilizes an exogenous photosensitizer that is preferentially absorbed by tumor cells, endothelial cells, and active inflammatory cells. Once the cells harboring the photosensitizer are irradiated with light fitting the absorption spectrum, the target cells are destroyed by production of ROS and execution of the apoptotic cascade.
PDT is used clinically to treat a wide range of medical conditions, including light-accessible premalignant and malignant cancers [104]. The most widely used photosenstizer is ALA, which can convert to porphyrins in the tissue [115]. Due to its potent effect in inducing lymphocyte apoptosis, extra-corporeal photopheresis is used to treat erythrodermic cutaneous lymphomas. Despite the introduction of several effective biological agents in medicine and dermatology, phototherapy remains a reliable and preferred option for treatment of several dermatological diseases.
MelanocytesMelanins, produced by melanocytes, play an important role in protecting the skin against UV radiation.
UV-induced DNA damage in melanocytes is more effectively prevented in darker skin due to an enhanced UV-induced apoptosis. The decrease of DNA damage with more efficient removal of UV-damaged cells may contribute at least in part to the decreased prevalence of skin cancers in individuals with dark skin [118]. On the other hand, once the melanocytes escape the apoptosis check, they can undergo malignant transformation to one of the most fatal cancers in the human, malignant melanoma [119].
In therapeutical applications, the narrow band UVB induce repigmentation in vitiligo by inhibition of self-destruction against external stresses [120] and by promotion of melanocyte regeneration [121,122].
ConclusionsUV radiation is absorbed by nuclear DNA, initiating a cascade of apoptotic events by forming DNA photoproducts and suppressing DNA synthesis.
UV radiation can also cause damage to the molecular targets located in the cytosol and cell membranes of keratinocytes. UV may result in the depletion of epidermal LCs and dermal T lymphocytes, which then lead to Treg activation in the lymph nodes.
The articles reviewed in this study suggest that DNA damage, induction of apoptosis, immune suppression, alteration in cytokine profiles, and induction of cell signaling pathways may contribute to the effects of UV-based phototherapy. Today different UVB sources, narrowband UVB lamps, a 308-nm UVB excimer laser, UVA or UVA1 lamps are widely applied for treatment of inflammatory, sclerosing, and neoplastic conditions including atopic dermatitis, sclerosing skin conditions such as morphea, vitiligo, and mycosis fungoides.
Understanding the detailed mechanisms through which phototherapy using different UV sources exert its effect as well as a better understanding of the pathophysiology of various diseases should help open up the paths for future therapeutic options.



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