Investigation of hepatoprotective effect of some algae species on carbon tetrachloride-induced liver injury in rats.

The aim of this study was to investigate hepatoprotective effect of some algae species such as Spirulina platensis, Chlorella vulgaris, Laminaria japonica, Sargassum sp. on experimental acute hepatotoxicity model that induced with carbon tetrachloride (CCl4) in rats. Algaes at a dose of 200 mg/kg and Silymarin at a dose of 25 mg/kg were orally administered for 7 days followed by CCl4 at a single dose (0.5 ml/kg), at the 8th day to cause experimental acute hepatotoxicity. Levels of biochemical (AST, ALT etc.), lipid peroxidation (MDA), antioxidant (GSH, CAT, GPx) parameters and histopathological examination were carried out to investigate the hepatoprotective effects of algae. In Sp group ALT and ALP levels were significantly decreased compared with CCl4 (p < .05). Histological liver structures of Sp group were similar to the control group. MDA, GPx and CAT levels of Sp and La groups were significantly different compared with CCl4 (p < .05). Based on these results, algae species able to minimise the toxic effects of CCl4 and especially S. platensis could be used in the purpose of protection against chemical-induced hepatotoxicity.

The protective effect of L-carnitine against hippocampal damage due to experimental formaldehyde intoxication in rats.

We investigated the protective effects of L-carnitine on hippocampus tissue damage in rats during experimental formaldehyde (FA) intoxication. Male Wistar albino rats were assigned into four groups: (1) control (C), (2) formaldehyde (FA), (3) formaldehyde + 0.5 g/kg of L-carnitine (FA + 0.5 LC) (4) formaldehyde + 1 g/kg L-carnitine (FA + 1 LC). At the end of the 14 day trial period, animals were sacrificed by decapitation under anesthesia. The hippocampus tissue samples were extracted to measure MDA, GSH and SOD activity. Neuronal degeneration was assessed based on histopathological (hematoxylin and eosin) and immunohistochemical (anti-ubiquitin) examination. To detect oxidative stress, specimens were reacted with anti-Cu/Zn-SOD antibody. After administering L-carnitine with FA to the animals, the activities of SOD and GSH increased, but the levels of MDA decreased in hippocampus tissue. Neuronal degeneration was observed in the FA group. L-carnitine administration reduced neuronal degeneration and histological structure was similar to controls. After FA application, degenerated hippocampus neurons were stained with anti-ubiquitin and Cu/Zn-SOD antibodies; weakly positive staining was observed in L- carnitine-treated groups. L-carnitine may be useful for preventing oxidative damage in the hippocampus tissue due to formaldehyde intoxication.

Immunohistochemical characterization of perineal melanoma in Kilis goats.

We describe the clinical, histopathological and immunohistochemical features of the malignant melanomas in the perineal regions of Kilis goats from Sanliurfa province in Turkey. We studied 13 female Kilis goats between 3 and 8 years old that were brought to Harran University Veterinary School, Department of Surgery, between 2002 and 2010. By macroscopic examination, the masses were determined to have elastic consistency, dark brown-black color, necrotic surfaces and ulceration. Microscopically, pleomorphic cells were observed under the basal layer and these advanced toward the dermis. These cells were polyhedral, round or spindle-shaped, anaplastic, and their cytoplasm contained varying amounts of dark brown-black pigments. Immunohistochemical staining was obtained with anti-melan A, vimentin and S100 antibodies.

Protective effect of L-carnitine on experimental lead toxicity in rats: a clinical, histopathological and immunohistochemical study.

Female Wistar-albino rats were given lead acetate (PbAc) for 60 days to investigate the protective effects of L-carnitine (CA) clinically and histopathologically on PbAc-induced tissue damage. Blood samples were obtained from the jugular vein for hemoglobin (HB), hematocrit (HCT), red blood cells (RBC), white blood cells (WBC), platelets (PLT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine. PbAc treatment caused a significant decrease in HB, HCT and RBC, a significant increase in WBC, AST, ALT and creatinine compared to controls. Although administration of CA did not reverse HB and HCT values, it reversed both the decrease in RBC and the increase in WBC, AST, ALT and creatinine. After the experimental period, all rats were weighed, then decapitated for pathological examination. Control rat liver, kidney and brain showed normal histological architecture. Lead-induced nephropathic kidneys; degenerative changes, inflammation and portal edema of the liver; and brain neuropil vacuolation, neuronal vacuolation, satellitosis and neuronophagia were observed in experimental groups. All changes were reduced in the PbAc group treated with CA (PbAc + CA). PbAc caused copper/zinc superoxide dismutase (Cu/Zn-SOD) expression in both the hepatocytes and tubular epithelium of the kidney. PbAc + CA exposure caused moderate Cu/Zn-SOD immunoreactivity. While in the brain sections of the PbAc group the degenerative neurons were stained intensely with anti-ubiquitin antibody, PbAc + CA rats showed moderate staining in neurons with anti-ubiquitin antibody. These results show that CA as a food additive reduced the severity of tissue damage caused by PbAc.