Protective effect of intravenous lipid emulsion treatment on malathion-induced ovarian toxicity in female rats.

OBJECTIVE: Malathion (MLT) is an organophosphate (OP) pesticide widely used in agriculture and for domestic purposes for several years. Intravenous lipid emulsion (ILE) has been reported to reduce toxicity caused by some lipid soluble agents. The aim of this study was to investigate the possible protective effects of ILE treatment on acute malathion toxicity in ovarian tissue of female rats. MATERIALS AND METHODS: Twenty-one adult female Wistar rats (weighted 200-250 g) were divided into three groups; control (corn oil, gavage), MLT (one administration of 100 mg/kg/ by gavage), 20% ILE (one intravenous administration of 3 ml/kg) plus the MLT group. Blood samples were collected for biochemical tests. The ovaries were removed and fixed for histopathological and immunohistochemical analyses. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were investigated in ovarian tissues. Histopathological and immunohistochemical evaluations were performed through scoring ovarian tissue damage and bax/caspase-3 immunoreactivity, respectively. RESULTS: SOD activity decreased in MLT group compared to the control group in tissue samples (p = 0.012). ILE treatment significantly increased SOD activity in MLT+ILE group compared to MLT group in tissue samples (p = 0.017). MLT treatment increased significantly caspase-3 and bax immunoreactivity while ILE decreased bax and caspase-3 immunoreactivity. However, no significant difference was found for MDA levels and GSH-Px activity in both blood and tissue samples and for histopathological results. CONCLUSIONS: The present study revealed that acute oral MLT administration increased oxidative stress and apoptosis in the rats. ILE treatment partially decreased deleterious effects of MLT. Further controlled animal studies are required to define the role of ILE in acute OP poisonings.

Significance of vitronectin and PAI-1 activity levels in carotid artery disease: comparison of symptomatic and asymptomatic patients.

AIM: Carotid atherosclerosis one of the main risk factors for ischemic stroke. Acute thrombosis after atherosclerotic plaque disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. PAI-1 is the most important and most rapidly acting physiological inhibitor of tissue-type (t-PA) and urokinase type (u-PA) plasminogen activators. Active PAI-1 form spontaneously converts to the latent with a half-life of ~1 h. Complex formation with vitronectin increases half life of PAI-1 by two- to four-folds. Thus, this inhibitor function of PAI-1 facilitated by Vn that binds the inhibitor and may regulate its activity by the stabilizing the active PAI-1 conformation. In addition, PAI-1/VN complexes may effect vascular structure and function. However, the exact role of these complexes in vascular remodelling are not completely clear. The aim of the present study was determining, correlating and comparing the plasma vitronectin, t-PA and PAI-1 activity levels in asymptomatic and symptomatic patients with carotid artery plaque. METHODS: A total of 37 carotid artery disease patients were included in this study. Blood samples were obtained from Cerrahpasa Medical School, Department of Heart and Vessel Surgery, University of Istanbul. Plasma vitronectin, tPA and PAI-1 activity levels were determined by ELISA. RESULTS: We found plasma PAI-1 activity levels were elevated in the asymptomatic group as compared with symptomatic group (P=0.038). We have also found a positive correlation between PAI-1 activity and vitronectin levels in symptomatic group (r=0.399, P=0.039). CONCLUSION: Decreased PAI-1 activity levels correlate with vitronectin in the symptomatic group; a) may be the consequence a compensatory mechanisms (due to possibilty in increased fibrinolytic activity and decreased vascular remodelling) against disease progression. b) or may be also cause progression of disease by increase of vascular remodelling.

The effects of different doses of melatonin on lipid peroxidation in diet-induced hypercholesterolemic rats.

This study aims to see in an animal experiment how differently the low and high doses of melatonin affect the antioxidant status and peroxidation of lipids. Forty-two male Wistar-Albino rats weighing about 200 gr (180-220) aged 6-7 months were used. Of these rats, 12 were fed with normal rat chow for 12 weeks. The latter ones were divided into two groups, each containing 6 rats. Group 1 (control group) received daily intraperitoneal injections of NaCl (0.9%; w/v). Group 2 was injected ethanol daily (4%; v/v; i.p.) to see the effects of ethanol in which we dissolved melatonin. Thirty rats were fed with a diet enriched with cholesterol (2%; w/w), cholic acid (0.5%; w/w) and propilthyouracil (0.5%; w/w) for 12 weeks. These rats were divided into three groups each containing 10 rats. The low-dose group received melatonin 1 mg/kg/d; i.p. (group 3), the high-dose group received melatonin in a dose of 10 mg/kg/d; i.p. (group 4), and only the cholesterol group did not get any vehicle (group 5). Total cholesterol (TC), LDL cholesterol (LDL-C), total antioxidant capacity (TAC), oxidized LDL (oLDL) and TBARS lelvels were measured in all groups. The produced high-cholesterol diet increased LDL cholesterol. Melatonin decreased the extent of this plasma lipoprotein increase and also prevented the oxidation of it. This effect was clearer when the dose was higher. Antioxidant status seems to be also dose-dependent (Tab. 2, Ref. 33).