Journal of Clinical Toxicology
Open Access
ISSN: 2161-0495
ISSN: 2161-0495
Gabriela Hollmann, Gabrielle de Jesus Ferreira, M�?¡rcio Alberto Geihs, Marcelo Alves Vargas, Luiz Eduardo Maia Nery, �?lvaro Leit�?£o, Rafael Linden and Silvana Allodi
Posters-Accepted Abstracts: J Clin Toxicol
Ultraviolet (UV) radiation can produce biological damage, principally oxidative stress, by increasing the production of reactive
oxygen species (ROS). This study evaluated biochemical impairments related to the oxidative stress induced by UVA, UVB and
UVA + UVB (Solar Simulator-SIM) in environmental doses, during five consecutive days of exposure, in the brain and eyestalk of
the crab Ucides cordatus. We evaluated these regions by sampling on the 1st, 3rd and 5th days of UV exposure for lipid peroxidation
(LPO), antioxidant capacity against the peroxyl radical (ACAP), and the activities of catalase (CAT), glutathione peroxidase (GPX)
and glutathione-s-transferase (GST). Immunohistochemical and immunoblotting assays were performed for anti-activated-caspase
3 in the brains. After the first day of exposure, LPO increased in the eyestalks and brains of the UV-exposed animals; ACAP, CAT,
GPX and GST also increased in the brains. On the third day, the LPO values in the eyestalk remained high in the UV-exposed groups,
while ACAP decreased in the brain and eyestalk and CAT remained high in all irradiated groups in both regions. On the fifth day,
LPO decreased in the eyestalk and brain of the UV-exposed groups. These results may have been a consequence of the ADS activity,
since CAT was high in both regions, ACAP was high in the eyestalks of the SIM group, and GPX remained high in the eyestalks of
the UVA and UVB groups. Immunohistochemical assays and immunoblotting showed that there was apoptosis in the brains of the
UV-exposed crabs. In conclusion, environmental doses of UV can cause oxidative damage to the CNS cells, including apoptosis.