IntroductionVitamin D is created in the skin after it has been treated with UVB radiation. It is metabolized first in the liver (as 25-hydroxyvitamin D), and then in the kidneys before it reaches an active state (1,25-dihydroxyvitamin D). Vitamin D allows the body to absorb more than ten percent of dietary calcium (Holick, 2007). Calcium is of vital importance to the body, contributing to immune function, bone formation and fortification, and the prevention of tetany (Deluca, 2004). Calcium is also imperative for proper heart function, and in the appropriate dosages may be able to stave off cardiovascular disease. During cardiac contraction calcium influx causes the plateau effect that occurs right after Sodium flows into the cell (depolarizing it and thus causing the action potential), and ends as Potassium ion flow out of the cell during repolarization, increases. Should a body be hypocalcemic the plateau effect would be lengthened (as a certain amount of Calcium must be attained before repolarization) and thus the heart rate of the body would slow (Netter 1992) As both chemical and physical sunscreens block out UV light to a certain degree, they should reasonably inhibit the absorption of Vitamin D, and thus have an effect on heart rate. The objective of this experiment is see if this phenomenon may be observe in mus musculus by treating them with sunscreen and radiating them with UV light as well as to differentiate the effects of chemical and physical sunscreen on heart rate. Materials and Methods12 mice were purchased from Sand Bar Pet Shop and tested in groups of 6. Two cages were bought from Petco to separate the mice (one Grey and one Turquoise). The mice were marked with 6 different colors: red, orange, blue, green, purple, and brown, at either the posterior or anterior ends of their tails depending on their cage. The mice were subjected to UVA and UVB light in accordance with the 12:1 allometric cell ratio between mice and Humans (FDA 2005) after which, heart rates were taken using the Pulse Plus heart rate monitor. Because the mice have suchwhite reflective fur 5 more seconds were added to the original 25 of UVA/UVB exposure they were to endure. UVB/UVA treatment lasted 5 days, with 4 day’s worthof recorded heart rates while the mice were on a Vitamin D poor diet (so as to make sure dietary vitamin D would not distort the results). This diet consisted of roasted soybeans (providing an adequate source of Ca+), dried mango, roasted sunflower seeds, apple chips and water. Mice were held until their heart rate reached its highest peak as shown by the Pulse Plus. Because the mice were so small the monitor had difficulty receiving the heart rate signals. To make sure the heart rates were taken consistently the heart monitor was allowed to reach 100 beats per minute regardless of the many drops and spikes it recorded as it was trying to calibrate to the mouse. After it reached 100 beats per minute the heart rate was not allowed to drop three times before the highest heart rate was recorded. One of the mice was presumed pregnant due to her significantly larger belly size and recorded mass and was removed from the study. Another mouse died one day into the testing.As both mice were from the same cage (turquoise), the blue mouse from the grey cage was transferred to create an even distribution of mice. After the last day of treatment a paired t-test was performed comparing the beginning heart rates to the heart rates “pre-sunscreen”. The mice were then separated into groups of 3. Each group was assigned a sunscreen: one chemical, and one physical, and the control (which would be beamed with UV but would not receive any sunscreen treatment). 30 SPF CVS brand titanium dioxide (9.1%) physical sunscreen and 30 SPF CVS brandChemical sunscreen were applied to the appropriate mice. Blue 2, the original blue marked mouse from the turquoise cage was removed from the study arbitrarily. After waiting 30 minutes for the sunscreen to soak in (shaking the cages when the mice tried to groom themselves) 30 seconds of UVA/UVB treatment commenced. After sunscreen treatment, mice were wiped down with Huggies Baby Wipes so as toprevent poisoning should they continue to groom themselves. Heart rates were again taken in the same manner for 2 days. An ANOVA and post Hoc tests were analyzed between the three groups.ResultsFigure 1. The Average heart rate taken at the beginning of the experiment on the first day of UV treatment compared to the last day of heart rate data; 127.6 ± 4.828618 and 127.1 ± 4.207005 respectively. A Paired two-tailed t-test displayed no significance difference between the two (P = 0.949419). Error bars indicate the standard error of the mean.Figure 2. Average heart rates of Chemical sunscreen treated, Physical sunscreen treated, and sunscreen untreated mice. The averages are 128±s.e., 120±s.e., and 132.67±s.e. Respectively. The ANOVA suggested no significant difference (P = 0.57671) between the groups. Error bars indicate standard error of the mean. Figure 3.DiscussionThe results of this experiment suggests no significant difference in heart rate between sunscreen treated mice and non-treated mice. It also suggests that there is no difference in Heart rate between chemically and physically sunscreen treated mice. There are several reasons why this may be the case. The mice have fur covering almost the entirety of their bodies, which is very different from the human skin condition. The amount of UV light exposure may not have been enough to significantly penetrate their fur. Heart Rates were difficult to measure as the mice consistently squirmed as they were being held (and seemed particularly terrified of the heart monitor). The Pulse Plus, which was made for a human finger, seemed to have difficulty picking up the mice heart rates, which may have also caused inaccurate readings. Other difficulties and unwanted variables arose with the mouse diet. The diet had to be created, however, prior to the purchase of the mice they wereall being fed a high vitamin D diet and, as vitamin D is generally stored when not used they may have maintained their heart rates by using there vitamin D reserves. Works citedAckerman, U. (2002). PrettyDarnQuick: Physiology. London, England: BC Decker Inc.Vitamin D. (2011). In National Institute of Health. Retrieved November 13, 2011Estimating the maximum safe starting dose in initial clinical trials therapeutics in adult healthy