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Carrying between February 2012 and February 2013 as seasonal, the present study aims to determine heavy metal loads of five different creeks pass through Giresun city center and disembogue to Black Sea. Heavy metal analyses were performed from selected stations by ICP-MS instrument. Without seasonal and station differences, metal levels were found as follow; Cd: 0.129-5.113, Mn: 0.009-2.937, Fe: 0.007-1.985, Cu: 0.002-1.344, Zn: 0.002-1.901, Ni: 0.003-0.149, Pb: 0.009-21.22, Cr: 0.002-0.177, Co: 0.001-0.087 mg/L in water. Cd: 0.118-166.3, Pb: 5.62-398.9, Mn: 111.7-988.2, Fe: 2919-117973, Cu: 18.60-963.9, Zn: 11.09-2471, Ni: 11.29-813.1, Cr: 10.76-860.5, Co: 8.59-757.1 mg/kg in sediment. There were statistically significant differences between seasons in sea water. Statistically differences were found on Aksu, Güre, and Batlama stations. In sediment, statically differences in Cu, Zn, Ni, Co levels were found in winter season. The same elements were also statistically different on Güre station.

Background: Plasminogen activator inhibitor-1 (PAI-1) antagonists are known for their neuroprotective effects. In this study, it was aimed to investigate the possible protective effects of PAI-1 antagonists in a rat mild traumatic brain injury (TBI) model. Method: Sprague Dawley male rats were grouped as sham (n=7), TBI (n=9), TBI + PAI-1 antagonist (5 and 10 mg/kg TM5441 and TM5484; n=6-7). Under anesthesia, TBI was induced by dropping a metal 300gram weight from a height of 1 meter on the skull. Before and 24-hour after trauma neurological examination, tail suspension, Y-maze, novel object recognition tests were performed. Twenty-four hours after TBI, the rats were decapitated and activities of myeloperoxidase, nitric oxide release, luminol-and lucigenin-enhanced chemiluminescence were measured. Also, interleukin-1b, interleukin-6, tumor necrosis factor, interleukin-10, tumor growth factor-b, caspase-3, cleaved caspase-3, and PAI levels were measured with the ELISA method in the brain tissue. Brain injury was graded histopathologically following hematoxylin-eosin staining. Western blot and immunohistochemical investigation for low-density lipoprotein receptor, matrix metalloproteinase-3 and nuclear factor-kB were also performed. Data were analyzed using GraphPad Prism 8.0 (GraphPad Software, San Diego, CA, USA) and expressed as means ± SEM. Values of p < 0.05 were considered to be statistically signi cant.Results: Higher levels of myeloperoxidase activity in the TBI group (p<0.05) were found to be suppressed in 5 and 10 mg/kg TM5441 treatment groups (p<0.05-p<0.01). The tail suspension test score was increased in the TBI group (p<0.001), and decreased in all treatment groups (p<0.05-0.001). The histologic damage score was increased statistically signi cantly in the cortex, dentate gyrus, and CA3 regions in the TBI group (p<0.01-0.001), decreased in the treatment groups in the cortex and dentate gyrus (p<0.05-0.001).Conclusion: PAI antagonists, especially TM5441, has antioxidant and anti-in ammatory properties against mild TBI in the acute period. Behavioral test results were also improved after PAI antagonist treatment after mild TBI. HighlightsAfter mild TBI, PAI-1 antagonists TM5441 and TM5484 was used for the rst time in the literature. PAI-1 inhibition reduced oxidative stress, in ammation and neuronal damage in a TBI model. PAI antagonist treatment also improved corticospinal pathway functions and behavioral results.

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