Effects of mentha spicata L. Extracts on hormonal regulation of energy metabolism in rats with hypercholesterolemia and hyperlipidemia

This study aimed to investigate the effects of Mentha spicata L. (Lamiaceae), which contains caffeic acid, rosmarinic acid, alpha tocopherol, and eugenol, on hormonal regulation of energy metabolism in rats. Obesity is a risk factor for various diseases such as hyperlipidemia, arteriosclerosis, and fatty degeneration in the liver. Furthermore, it has been aimed to inquire the effect of the Mentha spicata L. whether it is effective as a liver protective factor in rats fed on high fat diet. In this study, 70 Wistar-Albino male rats aged 2±3 months were used. The animals were allocated into 7 groups (10 rats in each group): 1 control group and 6 experimental groups, including negative control; carboxymethyl cellulose (CMC); high-fat diet, positive (HFD); M. spicata petroleum ether extract (PE); M. spicata ethyl acetate (EtOAc) extract; and M. spicata methanol (MeOH) extract. All experimental groups were given dietary fat and M. spicata extracts, excluding the control group. The group C rats were fed the standard rat diet; group CMC high-fat diet (40% beef tallow + 1% cholesterol) + 1 mL 0.5% CMC; group HFD high-fat diet; and groups PE, EtOAc, and MeOH petroleum ether, ethyl acetate, and methanol extracts of M. spicata, respectively, via gastric gavage for 60 days. The plasma concentrations of hormones [leptin, ghrelin, adiponectin, insulin, and thyroid hormones (T4, FT4, T3, and FT3)], glucose, aspartate aminotransferase, alanine aminotransferase, total protein, and lipid profiles (cholesterol, low-density lipoprotein, high-density lipoprotein, and triglycerides) were monitored. The histopathologic examination revealed fatty degeneration in the liver tissue and perivascular accumulation of inflammatory cells in the experimental groups. The PE extract obtained from M. spicata was effective in maintaining the body weight and protecting against liver degeneration. Further studies are required to verify this. © 2019 Parlar Scientific Publications. All rights reserved

The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats: The protective role of resveratrol

The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks. In total, 48 Wistar rats were used and divided equally into six groups. The groups were designed as the control group (received only a rodent diet and tap water), the corn oil group (0.5 ml corn oil by the oral route), and the malathion group (100 mg kg-1 day-1 by the oral route). Other three groups received malathion (100 mg kg-1 day-1) plus Res (5, 10, and 20 mg kg-1 day-1, respectively) by the oral route. Malathion increased malondialdehyde and 8-OHdG levels, whereas it decreased glutathione levels. Also, acetylcholinesterase, superoxide dismutase, and catalase activities were found to be low in the blood, liver, kidney, heart, and brain tissues. Biochemical parameters were not notably changed in all groups. In contrast, Res treatment inverted malathion-induced oxidative stress, lipid peroxidation, and activity of enzymes. Additionally, malathion-induced histopathological changes in the liver, kidney, heart, and brain were ameliorated by Res treatment. These results demonstrate that malathion increases oxidative stress and decreases the antioxidant status while Res has a protective function against malathion toxicity in rats. © The Royal Society of Chemistry.National Council for Scientific Research: BAPK-2012/MF003EA is grateful to Uşak University Scientific Research Council, Uşak, Turkey for providing financial support (Project no: BAPK-2012/MF003). IK thanks Afyon Kocatepe University, Faculty of Veterinary Medicine, Department of Biochemistry for providing laboratory facilities. Also, this study was orally presented at the 2nd International Congress on Advances in Veterinary Sciences and Technics, Skopje, Macedonia

Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats

PubMed ID: 25342379Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2?-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats. © 2014 Informa Healthcare USA, Inc.2012/MF003The authors declare that they have no conflicts of interest associated with this work. This study was supported by a grant from the Usak University Scientific Research Council, Usak, Turkey (Project no.: 2012/MF003)

Protective effects of boron on cyclophosphamide induced lipid peroxidation and genotoxicity in rats

PubMed ID: 24530163The aim of the present study was to evaluate the possible protective effect of boron (B) on cyclophosphamide (CYC) induced oxidative stress in rats. Totally, thirty Wistar albino male rats were fed standard rodent diet and divided into 5 equal groups: physiological saline was given intraperitoneally (i.p.) to the control group (vehicle treated), to the second group only 75mgkg-1 CYC was given i.p. on the 14th d, and boron was administered (5, 10, and 20mgkg-1, i.p.) to the other groups for 14 d and CYC (75mgkg-1, i.p.) on the 14th d. CYC caused increase of malondialdehyde and decrease of glutathione levels, decrease of superoxide dismutase activities in erythrocyte and tissues, decrease of erythrocyte, heart, lung, and brain catalase, and plasma antioxidant activities. Also, CYC treatment caused to DNA damage in mononuclear leukocytes. Moreover, B exhibited protective action against the CYC-induced histopathological changes in tissues. However, treatment of B decreased severity of CYC-induced lipid peroxidation and genotoxicity on tissues. In conclusion, B has ameliorative effects against CYC-induced lipid peroxidation and genotoxicity by enhancing antioxidant defence mechanism in rat. © 2014 Elsevier Ltd