Evaluation of the effects of Cyclotrichium niveum on brain acetylcholinesterase activity and oxidative stress in male rats orally exposed to lead acetate.

Cyclotrichium niveum is an endemic plant for Turkey and it appears to have in vitro antioxidant and acetylcholinesterase inhibition properties. To the best of our knowledge, there has been no study on the in vivo effects of this plant. Therefore, the purpose of this study was to evaluate the effects of C. niveum on lead (Pb)-acetate-induced potential alterations in brain acetylcholinesterase activity, as well as oxidative stress in male rats. The rats were randomly assigned to control, Pb-acetate, C. niveum and Pb-acetate+ C. niveum groups. Pb-acetate was provided in drinking water (500 ppm), and C. niveum was administered via orogastric gavage (4 ml/kg) for 30 days. The acetylcholinesterase activity in the brain significantly decreased only in the Pb-acetate group. The malondialdehyde level significantly increased, and the reduced glutathione activity decreased in the Pb-acetate group. The reduced glutathione and glutathione-S-transferase activities of the C. niveum group were higher than the control group. No Pb was detected on a ppb level in the brain tissue of the control and C. niveum groups, while it was detected in the brains of the rats in the Pb-acetate and Pb-acetate+ C. niveum groups (185+8.98 ppb and 206+56.65 ppb, respectively). The data collected in this study suggested that C. niveum may reduce inhibition of brain AChE activity and oxidative stress against Pb-acetate-induced alterations in the brain of male rats.

Role of geraniol against lead acetate-mediated hepatic damage and their interaction with liver carboxylesterase activity in rats.

In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.

Investigation of the effect of naringenin on oxidative stress-related alterations in testis of hydrogen peroxide-administered rats.

Testis tissue is prone to oxidation because its plasma membrane contains many polyunsaturated fatty acids. Naringenin is a plant-derived natural flavonoid. We investigated the possible ameliorative role of naringenin on the hydrogen peroxide (H2 O2 )-induced testicular damage in Wistar rats. Animals received 12 mg/kg H2 O2 by intraperitoneal injection, and 50 mg/kg naringenin via orogastric gavage for 4 weeks. In the H2 O2 group, the testis malondialdehyde level increased, while the amount of reduced glutathione, glutathione transferase activities, and the testis weight decreased. There were severe testicular damages in the H2 O2 group otherwise their grade were less in the naringenin + H2 O2 group. However, the serum testosterone concentrations decreased in both the H2 O2 and the naringenin + H2 O2 groups. The testicular zinc and calcium levels reduced in the H2 O2 -treated rats. In conclusion, the administration of H2 O2 caused oxidative stress in the testes and naringenin supplementation decreased the H2 O2 -induced effects, except for changes in testosterone levels.

Investigation of the role of α-lipoic acid on fatty acids profile, some minerals (zinc, copper, iron) and antioxidant activity against aluminum-induced oxidative stress in the liver of male rats.

BACKGROUND: We have investigated the effects of α-lipoic acid (LA), a powerful antioxidant, on the fatty acid (FA) profiles, aluminum accumulation, antioxidant activity and some minerals such as zinc, copper and iron against aluminum chloride (AlCl3)-induced oxidative stress in rat liver. METHODS: Twenty-eight male Wistar rats were divided into four groups as control, LA, AlCl3 and LA+AlCl3. For 30 days, LA was intraperitoneally administrated (50 mg/kg) and AlCl3 was given via orogastric gavage (1600 ppm) every other day. RESULTS: AlCl3-treated animals exhibited higher hepatic malondialdehyde concentration and lower glutathione peroxidase and catalase activity, whereas these alterations were restored by the LA supplementation. Total saturated FA of the AlCl3-treated group was higher than the LA supplementation groups. Moreover, total unsaturated FA level of the LA+AlCl3 group was higher than the AlCl3-treated group. Hepatic zinc level of the AlCl3-treated group was lower than the control group, whereas it was higher in the LA and the LA+AlCl3 groups. Hepatic copper levels did not significantly change in the experimental groups. Iron level was lower in the LA and LA+AlCl3 groups compared with the AlCl3-treated group. Moreover, the liver Al concentration was found to be lower in the LA and LA+AlCl3 groups compared to the AlCl3 group. CONCLUSIONS: These results indicate that AlCl3 treatment can induce oxidative stress in the liver. LA supplementation has a beneficial effect on the AlCl3-induced alterations such as high lipid peroxidation, Al accumulation, FA profile ratios and mineral concentrations.

A compound heterozygous EARS2 mutation associated with mild leukoencephalopathy with thalamus and brainstem involvement and high lactate (LTBL).

Mitochondrial glutamyl-tRNA synthetase is a major component of protein biosynthesis that loads tRNAs with cognate amino acids. Mutations in the gene encoding this enzyme have been associated with a variety of disorders related to oxidative phosphorylation. Here, we present a case of leukoencephalopathy with thalamus and brainstem involvement and high lactate (LTBL) presenting a biphasic clinical course characterized by delayed psychomotor development and seizure. High-throughput sequencing revealed a novel compound heterozygous mutation in mitochondrial glutamyl-tRNA synthetase 2 (EARS2), which appears to be causative of disease symptoms.

Effects of intraperitoneally administered ubiquinone on the level of total lipid and fatty acids in rat liver.

The purpose of the present study was to evaluate the effect of ubiquinone (coenzyme Q-10) on total lipid and fatty acid composition of liver tissues in rats. Twenty male wistar rats were randomly divided into two groups. The first group was used as a control. The second group received ubiquinone (8 mg/every other day) intraperitoneally. This administration was done for a period of 38 days. Body weight increases in animals fed diets for 38 days were on average 35 g in control group (C), and only 11 g in the ubiquinone group. Total lipid content of liver tissues in the ubiquinone group (UB) decreased significantly (p < 0.0001) compared to the control group (C). The ratio of 22:6 and total omega3 fatty acid in the UB increased (p < 0.01) compared to C. While the level of oleic acid (18:1), palmitoleic acid (16:1) and total monounsaturated fatty acid (MUFA) in UB significantly decreased (p < 0.01, p < 0.001, p < 0.001, respectively), the level of stearic acid (18:0) in liver tissue increased (p < 0.05) in the same group when compared to C. Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the synthesis of monounsaturated fatty acid mainly oleate (18:1). We speculate that ubiquinone inhibits SCD activity. SCD is an important metabolic control point in body weight regulation. Our results indicate that ubiquinone supplementation may have an inhibitory effect on obesity and it seems that the level of 22:6 in liver increased due to ubiquinone.