S [20]. The liver serves as the major target organ for PFOA
S [20]. The liver serves as the key target organ for PFOA, which causes an elevated liver weight, hepatocytic hypertrophy, hepatic triglyceride accumulation, multifocal coagulation, and liquefaction necrosis in rodents [8, 21, 22]. Furthermore, PFOA exposure increases the incidence of malignant hepatocellular2 carcinoma in rats [23]. Although considerable numbers of studies have reported the adverse effects of PFOA exposure around the liver, the underlying mechanisms haven’t however been fully elucidated. Many environmental contaminants have been reported to induce oxidative stress and to result in hepatic injury in experimental animals [246]. Additionally, extreme environmental pollutants have already been implicated to induce hepatic inflammation [279]. For that reason, the present study was designed to ascertain whether PFOA-induced hepatic toxicity was involved in oxidative stress and inflammatory response.16 Relative liver weight ( of body weight)BioMed Research Internationala 12 c eight d 4 b2. Supplies and Methods2.1. Animals. Male Kunming (KM) mice weighing 202 g had been purchased from the Laboratory Animal Center of Nanchang University. Mice had been maintained at 22 2 C and relative humidity (50 10 ) having a 12 h lightdark cycle and acclimatized for 1 week before the begin from the experiment. All animal procedures have been performed in accordance with all the Guidelines for Care and Use of Laboratory Animals of Nanchang University and authorized by the Animal Ethics Committee of Nanchang University. two.2. Therapies. PFOA (96 purity, Sigma-Aldrich, USA) was Coccidia custom synthesis dissolved in dimethyl sulfoxide (DMSO). Mice were orally administered distinctive concentrations of PFOA (two.5, 5, or 10 mgkgday) once everyday for 14 consecutive days. Controls received an equivalent volume of DMSO. At the finish of treatment period, the mice have been sacrificed immediately after anesthesia with sodium pentobarbital. Blood samples have been collected and livers have been aseptically excised and weighed. Liver tissues were fixed in 4 paraformaldehyde for histological examination or frozen in liquid nitrogen after which stored at -80 C for biochemical analyses. two.three. Measurement of Serum Enzymes. The blood samples were centrifuged at 13,000 rpm at 4 C for 30 min to separate serum. The activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and total bile acids (TBA) had been determined using a biochemical analyzer (7180, HITACHI, Japan). 2.four. Histology. The fixed liver samples have been dehydrated in ethanol HSP Formulation gradient options, embedded in paraffin, and sectioned at five m. The sections were stained with hematoxylin and eosin and observed below an optical microscope (IX71 Olympus, Japan). 2.5. Measurement of Malondialdehyde (MDA) and Hydrogen Peroxide (H2 O2 ). The levels of MDA and H2 O2 in liver tissue homogenates had been measured utilizing commercial kits (Jiancheng Institute of Biotechnology, Nanjing, China), in accordance using the manufacturers’ guidelines. The analyses were performed with a UV 1800 spectrophotometer (Shimadzu, Japan).2.PFOA (mgkg)Figure 1: Relative liver weight right after exposure to diverse concentrations of PFOA. Values are expressed as mean SEM ( = four). Bars with different letters are statistically distinctive ( 0.05).two.6. Measurement of Interleukin 6 (IL-6), Cyclooxygenase-2 (COX-2), and C-Reactive Protein (CRP). The frozen liver tissue was homogenized with ice-cold saline. The levels of IL-6, COX-2, and CRP in liver tissue homogenates have been determ.