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Effect of light irradiation and sex hormones on jurkat T cells: 17beta-estradiol but not testosterone enhances UVA-induced cytotoxicity in Jurkat lymphocytes.

Cohly HH, Graham-Evans B, Ndebele K, Jenkins JK, McMurray R, Yan J, Yu H, Angel MF - Int J Environ Res Public Health (2005)

Bottom Line: The effects of EST and TE were investigated between 1 and 20 ng/mL.We found that EST alone, without UVA, enhanced Jurkat T cell survival.Since TE did not alter cell viability in the presence of UVA further damaging studies were not performed.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Division of Plastic Surgery, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi, 39216-4505, USA. hcohly2004@yahoo.com

ABSTRACT
In Eastern cultures, such as India, it is traditionally recommended that women but not men cover their heads while working in the scorching sun. The purpose of this pilot study was to determine whether there was any scientific basis for this cultural tradition. We examined the differential cytotoxic effects of ultraviolet A light (UVA) on an established T cell line treated with female and male sex hormones. CD4+ Jurkat T cells were plated in 96 well plates at 2 x 106 cells/ml and treated with 17beta-estradiol (EST) or testosterone (TE). These cells were irradiated by UVA light with an irradiance of 170 J/cm2 for 15min at a distance of 6 cm from the surface of the 96-well plate. Controls included cells not treated with hormones or UVA. The effects of EST and TE were investigated between 1 and 20 ng/mL. Cytotoxicity by fluorescein-diacetate staining and COMET assay generating single strand DNA cleavage, tail length and tail moment measurements were examined. The effect of estrogen (5ng/mL) on apoptosis and its mediators was further studied using DNA laddering and western blotting for bcl-2 and p53. We found that EST alone, without UVA, enhanced Jurkat T cell survival. However, EST exhibited a dose-related cytotoxicity in the presence of UVA; up to 28% at 20 ng/ml. TE did not alter UVA-induced cytotoxicity. Since TE did not alter cell viability in the presence of UVA further damaging studies were not performed. COMET assay demonstrated the harmful effects of EST in the presence of UVA while EST without UVA. had no significant effect on the nuclear damage. Apoptosis was not present as indicated by the absence of DNA laddering on agarose gel electrophoresis at 5ng/ml EST or TE +/- UVA. Western blot showed that estrogen down regulated bcl-2 independently of UVA radiation while p53 was down regulated in the presence of UVA treatment. EST and TE have differential effects on UVA-induced cytotoxicity in Jurkat T-lymphocyte which suggested that women may be more susceptible to the harmful effects of solar irradiation than men.

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This figure represents the mechanism of action of estrogen. Under the influence of UVA radiation estrogen causes increased T cytotoxicity which results in increased DNA damage and decreased p53.
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f9-ijerph-02-00156: This figure represents the mechanism of action of estrogen. Under the influence of UVA radiation estrogen causes increased T cytotoxicity which results in increased DNA damage and decreased p53.

Mentions: DNA damage caused by UV radiation, which if left un-repaired, results in molecular alterations in the skin and blood which eventually lead to skin mutations found in skin cancer. Skin biopsies, as well as blood samples when taken after a single UV exposure were tested for p-53. Specifically, the study analyzed the amount of p53 protein in the skin and blood. Within 24 hours of the first UV exposure, p53 protein was present in all layers of the epidermis [34]. The increased presence of p53 protein in the skin signifies that the body is responding to the cell damage due to UV exposure. p53 is a protein which allows cells to slow down their reproduction process so that damage from UV radiation can be repaired [35–36]. Though the body is trying to repair the damage, there is the risk of a mistake in the repair process, which increases as the number of altered cells multiply. If there is a ‘miss’ in the cell repair process, subsequent replication of the altered cell may yield a clone of abnormal cells which may eventually appear as a skin cancer. The p53 tumor suppressor plays a key role in protection from the effects of different physiological stresses (DNA damage, hypoxia, etc.), and loss of its activity has dire consequences, such as cancer [36, 37]. In our study we found that estrogen up-regulates the expression of p53, but that p53 is down- regulated in the presence of UVA. Thus, the absence of p53 exhibits a decrease in defence mechanisms of T cells in the presence of estrogen when exposed to 15 minutes of UVA radiation. The mechanism of action of UVA radiation is depicted in Figure 9.


Effect of light irradiation and sex hormones on jurkat T cells: 17beta-estradiol but not testosterone enhances UVA-induced cytotoxicity in Jurkat lymphocytes.

Cohly HH, Graham-Evans B, Ndebele K, Jenkins JK, McMurray R, Yan J, Yu H, Angel MF - Int J Environ Res Public Health (2005)

This figure represents the mechanism of action of estrogen. Under the influence of UVA radiation estrogen causes increased T cytotoxicity which results in increased DNA damage and decreased p53.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3814710&req=5

f9-ijerph-02-00156: This figure represents the mechanism of action of estrogen. Under the influence of UVA radiation estrogen causes increased T cytotoxicity which results in increased DNA damage and decreased p53.
Mentions: DNA damage caused by UV radiation, which if left un-repaired, results in molecular alterations in the skin and blood which eventually lead to skin mutations found in skin cancer. Skin biopsies, as well as blood samples when taken after a single UV exposure were tested for p-53. Specifically, the study analyzed the amount of p53 protein in the skin and blood. Within 24 hours of the first UV exposure, p53 protein was present in all layers of the epidermis [34]. The increased presence of p53 protein in the skin signifies that the body is responding to the cell damage due to UV exposure. p53 is a protein which allows cells to slow down their reproduction process so that damage from UV radiation can be repaired [35–36]. Though the body is trying to repair the damage, there is the risk of a mistake in the repair process, which increases as the number of altered cells multiply. If there is a ‘miss’ in the cell repair process, subsequent replication of the altered cell may yield a clone of abnormal cells which may eventually appear as a skin cancer. The p53 tumor suppressor plays a key role in protection from the effects of different physiological stresses (DNA damage, hypoxia, etc.), and loss of its activity has dire consequences, such as cancer [36, 37]. In our study we found that estrogen up-regulates the expression of p53, but that p53 is down- regulated in the presence of UVA. Thus, the absence of p53 exhibits a decrease in defence mechanisms of T cells in the presence of estrogen when exposed to 15 minutes of UVA radiation. The mechanism of action of UVA radiation is depicted in Figure 9.

Bottom Line: The effects of EST and TE were investigated between 1 and 20 ng/mL.We found that EST alone, without UVA, enhanced Jurkat T cell survival.Since TE did not alter cell viability in the presence of UVA further damaging studies were not performed.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Division of Plastic Surgery, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi, 39216-4505, USA. hcohly2004@yahoo.com

ABSTRACT
In Eastern cultures, such as India, it is traditionally recommended that women but not men cover their heads while working in the scorching sun. The purpose of this pilot study was to determine whether there was any scientific basis for this cultural tradition. We examined the differential cytotoxic effects of ultraviolet A light (UVA) on an established T cell line treated with female and male sex hormones. CD4+ Jurkat T cells were plated in 96 well plates at 2 x 106 cells/ml and treated with 17beta-estradiol (EST) or testosterone (TE). These cells were irradiated by UVA light with an irradiance of 170 J/cm2 for 15min at a distance of 6 cm from the surface of the 96-well plate. Controls included cells not treated with hormones or UVA. The effects of EST and TE were investigated between 1 and 20 ng/mL. Cytotoxicity by fluorescein-diacetate staining and COMET assay generating single strand DNA cleavage, tail length and tail moment measurements were examined. The effect of estrogen (5ng/mL) on apoptosis and its mediators was further studied using DNA laddering and western blotting for bcl-2 and p53. We found that EST alone, without UVA, enhanced Jurkat T cell survival. However, EST exhibited a dose-related cytotoxicity in the presence of UVA; up to 28% at 20 ng/ml. TE did not alter UVA-induced cytotoxicity. Since TE did not alter cell viability in the presence of UVA further damaging studies were not performed. COMET assay demonstrated the harmful effects of EST in the presence of UVA while EST without UVA. had no significant effect on the nuclear damage. Apoptosis was not present as indicated by the absence of DNA laddering on agarose gel electrophoresis at 5ng/ml EST or TE +/- UVA. Western blot showed that estrogen down regulated bcl-2 independently of UVA radiation while p53 was down regulated in the presence of UVA treatment. EST and TE have differential effects on UVA-induced cytotoxicity in Jurkat T-lymphocyte which suggested that women may be more susceptible to the harmful effects of solar irradiation than men.

Show MeSH
Related in: MedlinePlus