Norma Osnaya Brizuela

Effect of oseltamivir on catecholamines and select oxidative stress markers in the presence of oligoelements in the rat brain

The effect that osteltamivir has on the metabolism of catecholamines and oxidative damage in the brains of young patients remains unclear. The purpose of this study was to measure the effects of oseltamivir, in the presence of oligoelements, on biogenic amines and select oxidative biomarkers in the brains of uninfected, young rats under normal conditions. The study was conducted using male Wistar rats intraperitoneally treated for three days with either a control dose of 0.9 % NaCl, oseltamivir (50 mg/kg), oligoelements (50 μL/rat), or oseltamivir (50 mg/kg) and oligoelements (50 μL/rat). The brain tissue extracted from the treated rats was used to determine the concentrations of adrenaline, noradrenaline, and dopamine, as well as the levels of GSH, lipid peroxidation, and ATPase activity. An increase in the concentration of adrenaline and noradrenaline and in the level of GSH in the group treated with oligoelements (p < 0.001) was observed, while the group treated with oseltamivir and oligoelements, the levels of dopamine increased (p < 0.001), and in the groups treated with oligoelements alone or combination with oseltamivir a decrease in lipid peroxidation was observed (p < 0.001). The results of this study suggest that the consumption of oseltamivir and oligoelements induce biphasic changes in the metabolism of catecholamines; thereby, inducing a protective mechanism against oxidative damage in the brains of young rats.

Effect of cerebrolysin on dopaminergic neurodegeneration of rat with oxidative stress induced by 3-nitropropionic acid

Abstract The study tested the hypothesis that cerebrolysin protects the brain from free radicals in rats treated with 3-nitropropionic acid (3-NPA). To address this hypothesis, the levels of dopamine (DA) and some oxidative stress biomarkers were measured after administration of 3-NPA. Young male Fischer rats were treated for three days with cerebrolysin, 3-NPA or both substances. Their brains were extracted, and DA, lipid peroxidation (LP), glutathione (GSH), calcium, and H2O2 were measured using validated methods. In the cortex, hemispheres and cerebellum/medulla oblongata of the group treated with cerebrolysin and 3-NPA, the levels of DA and LP decreased. In addition, calcium and H2O2 levels decreased in the hemispheres of the same group, while GSH increased in cortex. The increased dopamine metabolism due to the administration of cerebrolysin led to increased formation of radical species and oxidative stress, especially when free radicals were generated by 3-NPA.

Biochemical and histological changes produced by sweeteners and cytarabine in the brain of young rats

OBJECTIVE The aim of this study was to evaluate the effect of splenda and stevia on dopamine and 5-HIAA levels, and some biomarkers of oxidative stress in the presence of cytarabine. METHODS Forty-eight young male Wistar rats each with a weight of 80 g (four weeks of age), distributed in six groups of eight animals each, were treated as follows: group 1, control (NaCl 0.9% vehicle); group 2, cytarabine (0.6 g/kg); group 3, stevia (0.6 g/kg); group 4, cytarabine + stevia; group 5, splenda; and group 6, cytarabine + splenda. Cytarabine was given intravenously (IV) while stevia and splenda were administered orally for five days, using orogastric tube. At the end of treatment, the animals were sacrificed and glucose levels in blood were measured. The brains were dissected for histological analysis and homogenated to measure levels of dopamine, lipid peroxidation (TBARS), serotonin metabolite (5-HIAA), Na+, K+ ATPase activity, and glutathione (GSH), using validated methods. RESULTS Sweeteners increased the glucose in animals that received cytarabine. Dopamine increased in cortex and decreased in striatum of animals that received stevia alone and combined with cytarabine. 5-HIAA decreased in striatum and cerebellum/medulla oblongata of animals that received sweeteners and cytarabine alone or combined. GSH increased in animals that received sweeteners and decreased with cytarabine. Lipoperoxidation decreased in groups that received sweeteners and cytarabine. Histopathological changes revealed marked degeneration of neuronal cells in animals treated with cytarabine. CONCLUSION These results show that sweeteners as stevia or splenda may lead to the onset of unfavorable changes in dopamine and 5-HIAA. Antioxidant effects may be involved. Besides, histological changes revealed marked lesions of neuronal cells in experimental animals treated with cytarabine.

Trace elements cause oxidative damage in the brain of rats with induced hypotension

Hypertension causes neuronal damage and apoptosis in the brain. Diazoxide is a drug used in the treatment of hypertension however, its effect on 5-hydroxyindole acetic acid (5-HIAA) and dopamine amines in adult animal models remains unclear. The purpose of this study was to determine the effect of oligoelements on 5-HIAA and dopamine in the brain of adult rats treated with diazoxide METHODS: Male Fisher rats (weight 250g) were treated as follows: Group I, NaCl 0.9% (control); group II, tracefusin® (1.5mL/rat); group III, diazoxide (20mg/rat) and group IV, tracefusin® (1.5mL/rat)+diazoxide (20mg/rat). All doses were intraperitoneally administered on daily basis for four consecutive days. After the last administration, the brain of the animals was obtained and dissected in cortex, hemispheres (striatum) and cerebellum/medulla oblongata to measure the levels of 5-HIAA, dopamine, lipid peroxidation and total ATPase activity through validated methods. RESULTS Dopamine and 5-HIAA levels decreased significantly in the group that received trace elements and diazoxide in the hemisphere regions, while in cerebellum/medulla oblongata, dopamine levels increased significantly in the groups that received diazoxide alone in. Lipid peroxidation in all brain regions increased significantly in the groups that received trace elements and diazoxide. ATPase dependent of calcium and magnesium decreased in the groups that received diazoxide alone or combined with trace elements in cerebellum/medulla oblongata regions. CONCLUSION The present results suggest that the use of trace elements and diazoxide alters metabolism of dopamine and 5-HIAA amines. Free radicals may be involved in this effect.

Oleic Acid Protects Against Oxidative Stress Exacerbated by Cytarabine and Doxorubicin in Rat Brain.

AIM The objective of this study was to analyze the effect of doxorubicin and cytarabine on biogenic amines and oxidative biomarkers in the brain of rats treated with oleic acid. METHODS Thirty-six Wistar rats distributed in 6 groups, were treated as follows: group 1 (control), NaCl 0.9%; group 2 doxorubicin (1mg/kg); group 3 cytarabine (70mg /kg); group 4 oleic acid (1500μl/kg); group 5 doxorubicin + oleic acid; group 6 cytarabine + oleic acid. All compounds were administered intraperitoneally for 5 days. The Rats were sacrificed after receiving the last administration and their brains were dissected in cortex, hemispheres, and cerebellum/medulla oblongata. Blood samples were obtained on sacrifice to assess the levels of glucose and triglycerides. In each brain region, lipoperoxidation (TBARS), H2O2, Na+, K+ ATPase, glutathione (GSH), serotonin metabolites (5-HIAA) and dopamine were measured using validated methods. RESULTS Cytarabine decreased the levels of dopamine, TBARS, GSH, H2O2 and ATPase in all regions. Doxorubicin combined with oleic acid increased the levels of GSH in cortex, and decreased ATPase in cerebellum/medulla oblongata. CONCLUSION These results suggest that the reduction of dopamine and oxidant effect during cytarabine treatment could result in brain injury but could be prevented by oleic acid supplementation.

Effect of two antiandrogens as protectors of prostate and brain in a Huntington's animal model.

The purpose of this work is to know the effect of flutamide and a novel synthetic steroid 3β-p-Iodobenzoyloxypregnan-4,16- diene-6,20-dione (IBP) on the levels of dopamine, 5-HIAA (5-hydroxyindole acetic acid), and some oxidative stress markers in animal model with Huntington disease. Thirty male Wistar rats divided in groups of 6 animals each were subjected to the following treatment: group A, 3-nitro propionic acid (3-NPA, as inducer of Huntington); group B, flutamide; group C, 3-NPA + flutamide; group D, IBP; and group E, 3-NPA + IBP. Treatment scheme for all groups were at 4 mg/kg/day administered intraperitoneally. The measurement of haemoglobin was carried out from blood while the concentrations of ATPase, 5α-reductase, reduced glutathione (GSH), calcium, H2O2, 5-HIAA, and dopamine were determined from brain and prostate tissues using validated methods. The results depicted a significant decrease of dopamine and GSH in cerebellum/Medulla oblongata of animals treated with IBP. The prostate gland of the same group of treatment also showed a significant decrease in the concentrations of TBARS, H2O2, and total ATPase. In hemispheres of groups D and E, dopamine, H2O2, and total ATPase decreased significantly while in prostate, hemispheres, and cerebellum/Medulla oblongata of groups B and C; calcium, 5α-reductase, ATPase, H2O2, and TBARS were found to witness a significant decrease. Results showed an antiandrogenic activity of flutamide, while the novel steroid IBP showed neuroprotective properties by changes on oxidative stress biomarkers as critical pathways leading to prostate and brain degeneration. Probably steroid homeostasis disequilibrium could have led to alterations in dopamine metabolism GSH in Huntingtons disease animal models.

Folic acid increases levels of GHS in brain of rats with oxidative stress induced with 3-nitropropionic acid

Abstract Aim: This study tested the hypothesis that folic acid (FA) modulates biogenic amines and protects the brain against oxidative stress induced by 3-nitropropionic acid (3NPA). Methods: Male Wistar rats received (groups of six) for 5 d: FA (50 mg/kg); 3NPA (10 mg/kg); or FA +3NPA. At last day, rats were sacrificed, and their brain was obtained to measure the levels of dopamine, 5-hydroxiindol acetic acid (5-HIAA). Reduced glutathione (GSH), total ATPase, H2O2 and lipid peroxidation were measured. Results: GSH increased significantly in cortex of rats treated with FA. ATPase increased significantly in cerebellum/medulla oblongata and decreased in cortex of animal treated with 3NPA. 5-HIAA increased in striatum of rats that received 3NPA alone or combined with FA. Conclusion: 3NPA generates free radicals such effect can be counteracted with FA administration since this folate increases antioxidant capacity and modulates biogenic amines.AbstractAim: This study tested the hypothesis that folic acid (FA) modulates biogenic amines and protects the brain against oxidative stress induced by 3-nitropropionic acid (3NPA).Methods: Male Wi...

Oseltamivir and indomethacin reduce the oxidative stress in brain and stomach of infected rats

The aim of this study was to determine the effect of oseltamivir and indomethacin on lipid peroxidation (LP), GABA levels, and ATPase activity in brain and stomach of normal and infected rats (IR), as novel inflammation model. Female Sprague Dawley rats grouped five each, either in the absence or presence of a live culture of Salmonella typhimurium (S. typh), were treated as follows: group 1 (control), PBS buffer; group 2, oseltamivir (100 mg/kg); group 3, indomethacin (67 μg/rat); group 4, oseltamivir (100 mg/kg) + indomethacin (67 μg/rat). All drugs were given intraperitoneally for 5 days. IR received the same treatments and the brain and stomach of the rats were removed in order to measure levels of GABA, LP, and total ATPase, using validated methods. Levels of GABA increased in stomach and cortex of IR with oseltamivir, but decreased in striatum and cerebellum/medulla oblongata of IR with indomethacin. LP decreased in the three brain regions of IR with oseltamivir. ATPase increased in stomach of IR and non‐IR with oseltamivir and in striatum and cerebellum/medulla oblongata of IR with indomethacin. Results suggest that the effect of free radicals produced in an infection and inflammatory condition caused by S. typh could be less toxic by a combination of oseltamivir and indomethacin.

Assessment of a Synthetic Steroid and Flutamide on Dopamine, GSH and H 2 O 2 Levels in Rat Brain in Presence of Fructose

UNLABELLED Flutamide is a drug used in the treatment of androgen-dependent disorders. However, this treatment is usually accompanied by some adverse side effects. The aim of this work was to analyse the effect of flutamide and to compare this effect with that of a synthetic steroid - 3β-propionyloxy-5-androsten-17-one (PPA) - on levels of dopamine and some oxidative stress markers. For this, thirty-six male young Wistar rats (65g) were recruited and divided into 6 groups. The groups were then treated as follows: Group 1 (control), dimethyl sulfoxide (DMSO); group 2, flutamide (4 mg/kg); group 3, PPA; group 4, DMSO + fructose; group 5, flutamide + fructose; and group 6, PPA + fructose. The treatments were administered intraperitoneally at a daily dose of 4 mg/kg for 10 days. In the last day of treatment, blood samples were obtained and used to assess the levels of glucose and cholesterol. The animals were then sacrificed and their prostate gland and brains were obtained for measurement of 5α-reductase, glutathione (GSH), calcium, H2O2, and dopamine in cortex, hemispheres, and medulla/oblongata, using previously validated methods. RESULTS Dopamine levels decreased while GSH increased significantly in cortex and hemispheres of animals that received PPA plus fructose. Also in the same group, GSH decreased in cerebellum/medulla oblongata when compared with control group. Peroxidation decreased significantly in all tissues of the groups, while ATPase activity witnessed a significant decrease in cortex and an increase in hemispheres of animal groups treated with flutamide and PPA both in combination with fructose. CONCLUSION The steroid, 3β-propionyloxy-5-androsten-17-one, may in part act as a neuroprotector mediated by the increase of GSH and decrease of H2O2. Besides, imbalance in steroid homeostasis may alter the metabolism of dopamine.