RESUMEN

Present study aimed to assess effect of pre-treatment with Mucuna pruriens seed extract and its bioactive molecule(s) on NMDAR and Tau protein gene expression in cerebral ischemic rodent model. Methanol extract of M. pruriens seeds was characterized by HPLC, and ß-sitosterol was isolated by flash chromatography. In vivo studies to observe the effect of pre-treatment (28 days) with methanol extract of M. pruriens seed and ß-sitosterol on the unilateral cerebral ischemic rat model. Cerebral ischemia induced by left common carotid artery occlusion (LCCAO) for 75 min (on day 29) followed by reperfusion for 12 h. Rats (n = 48) divided into four groups. GroupI (control,Untreated + LCCAO)-No pre-treatment + cerebral ischemia; GroupII(ß-sitosterol + Sham)-pre-treatment with ß-sitosterol, 10 mg/kg/day + sham-operated; GroupIII(ß-sitosterol + LCCAO)-pre-treatment with ß-sitosterol, 10 mg/kg/day + cerebral ischemia; GroupIV(methanol extract + LCCAO)-pre-treatment with methanol extract of M. pruriens seeds, 50 mg/kg/day + cerebral ischemia. Neurological deficit score was assessed just before sacrifice. Experimental animals were sacrificed after 12 h reperfusion. Brain histopathology was performed. Gene expression of NMDAR and Tau protein of left cerebral hemisphere (occluded side) was performed by RT-PCR. Results revealed that the neurological deficit score was lower in groups III and IV compared to group I. NMDAR and tau protein mRNA expression in left cerebral hemisphere were upregulated in Group I, downregulated in groups III and IV. Histopathology of left cerebral hemisphere (occluded side) in Group I showed features of ischemic brain damage. Groups III and IV, left cerebral hemisphere showed less ischemic damage compared GroupI. Right cerebral hemisphere showed no areas of ischemia-induced brain changes. Pre-treatment with ß-sitosterol and methanol extract of M. pruriens seeds may reduce ischemic brain injury following unilateral common carotid artery occlusion in rats.

RESUMEN

Objective: Snake bite-induced elevation of serum LDH and CRP-1 is considered as useful biomarkers of hemotoxic. The snake venom contains proteins and may result in various envenomation such as bleeding, inflammation, and pain, cytotoxic, cardiotoxic, or neurotoxic effects. This in silico study was aimed to screen the snake venom proteins and to find out the most interactive hemotoxic venom protein against LDH and CRP-1 proteins as biomarkers. Materials and Methods: To validate the hypothesis of the prospective interaction of snake venom proteins, molecular docking analysis was used in the current work by deploying a cutting-edge docking program. Snake venom peptides were screened from literature and both peptide as well as target protein were obtained from PDB. HDOCK online server was used for the molecular docking analysis of target proteins with hemotoxic snake venom peptides. Further, the toxicity properties of each docked complex of target proteins were subjected for ADME/T analysis. Results: The selected snake venom peptides were subjected to molecular docking study and the results generated from computational-based approach reveals that all the hematotoxin snake venom proteins are interactive with LDH and CRP-1 peptide. Further, this study indicates that snake venom metalloproteinase (SVMPS) peptide may be considered as the best interactive protein with both LDH and CRP-1 proteins; also, ADME/T screening revealed that all docked complex are safe and follow toxicity properties. Conclusion: This in silico study clearly shows that the greatest interaction of SVMPS peptide with LDH and CRP-1 may be due to strong binding in the active site of the target proteins LDH and CRP-1 with SVMPS. Results, further, confirmed LDH and CRP-1 as potential biomarkers against hemotoxic snake venoms. This study should be validated by in vitro and in vivo analysis as well as specific species snake venom should be assessed. For further studies, SVMPS can be consider as therapeutic point of view.

RESUMEN

BACKGROUND: Nickel activates the signaling pathways through the oxygen sensing mechanism and the signaling cascades that control hypoxia-inducible transcriptional gene expressions through oxidative stress. This review emphasizes on the recent updates of nickel toxicities on oxidant and antioxidant balance, molecular interaction of nickel and its signal transduction through low oxygen microenvironment in the in-vivo physiological system. DISCUSSION: Nickel alters intracellular chemical microenvironment by increasing ionized calcium concentration, lipid peroxidation, cyclooxygenase, constitutive nitric oxide synthase, leukotriene B4, prostaglandin E2, interleukins, tumor necrosis factor-α, caspases, complement activation, heat shock protein 70 kDa and hypoxia-inducible factor-1α. The oxidative stress induced by nickel is responsible for the progression of metastasis. It has been observed that nickel exposure induces the generation of reactive oxygen species which leads to the increased expression of p53, NF-kß, AP-1, and MAPK. Ascorbic acid (vitamin C) prevents lipid peroxidation, oxidation of low-density lipoproteins and advanced oxidation protein products. The mechanism involves that vitamin C is capable of reducing ferric iron to ferrous iron in the duodenum, thus the availability of divalent ferrous ion increases which competes with nickel (a divalent cation itself) and reduces its intestinal absorption and nickel toxicities. CONCLUSION: Reports suggested the capability of ascorbic acid as a regulatory factor to influence gene expression, apoptosis and other cellular functions of the living system exposed to heavy metals, including nickel.

Asunto(s)

RESUMEN

Toxic metals, including excessive levels of essential metals tend to change biological structures and systems into either reversible or irreversible conformations, leading to the derangement of organ functions or ultimate death. Nickel, a known heavy metal is found at very low levels in the environment. Nickel is available in all soil types and meteorites and also erupts from volcanic emissions. In the environment, nickel is principally bound with oxygen or sulfur and forms oxides or sulfides in earth crust. The vast industrial use of nickel during its production, recycling and disposal has led to widespread environmental pollution. Nickel is discharged into the atmosphere either by nickel mining or by various industrial processes, such as power plants or incinerators, rubber and plastic industries, nickel-cadmium battery industries and electroplating industries. The extensive use of nickel in various industries or its occupational exposure is definitely a matter of serious impact on human health. Heavy metals like nickel can produce free radicals from diatomic molecule through the double step process and generate superoxide anion. Further, these superoxide anions come together with protons and facilitate dismutation to form hydrogen peroxide, which is the most important reason behind the nickel-induced pathophysiological changes in living systems. In this review, we address the acute, subchronic and chronic nickel toxicities in both human and experimental animals. We have also discussed nickel-induced genotoxicity, carcinogenicity, immunotoxicity and toxicity in various other metabolically active tissues. This review specifically highlighted nickel-induced oxidative stress and possible cell signaling mechanisms as well.

Asunto(s)

RESUMEN

BACKGROUND: Kenaf (Hibiscus cannabinus Linn, Pundi), Chick pea (Cicer arietinum Linn, Chana) and Prickly lettuce (Lactuca scariola Linn, Hattaraki) leaves are a few of indigenous plants which are routinely consumed by the people of north Karnataka in the diet. Studies on these plants showed some potential anti-diabetic efficacies. OBJECTIVES: To examine the effect of leaves extracts of Hibiscus cannabinus Linn, Cicer arietinum Linn and Lactuca scariola Linn on cardiovascular integrity, glucose homeostasis and oxygen sensing cell signaling mechanisms in alloxan induced diabetic rats. METHOD: In vitro and in vivo tests on glucose regulatory systems and molecular markers such as - NOS3, HIF- 1α and VEGF were conducted in alloxan induced diabetic rats supplemented with all the three plant extracts. Electrophysiological analysis (HRV, LF: HF ratio, baroreflex sensitivity, BRS) and histopathogy of myocardial tissues and elastic artery were evaluated in diabetic rats treated with L. scariola linn. RESULTS: Out of these three plant extracts, Lactuca scariola Linn supplementation showed significant beneficial effects on glucose homeostasis and oxygen sensing cell signaling pathways in alloxaninduced diabetic rats. Furthermore, effects of sub chronic supplementation of Lactuca scariola Linn aqueous extracts showed significant improvement in sympatho-vagal balance in diabetic rats by increase of Heart Rate Variability (HRV) and regaining of Baroreflex Sensitivity (BRS). These results were also corroborated with myocardial and elastic artery histopathology of Lactuca scariola Linn supplemented diabetic rats. CONCLUSION: These findings indicate an adaptive pathway for glucose homeostasis, oxygen sensing cell signaling mechanisms and cardio protective actions in alloxan - induced diabetic rats supplemented with Lactuca scariola Linn extracts.

Asunto(s)

RESUMEN

Groundwater fluoride concentration and fluoride-related health problems were studied in twenty-two villages of Indi taluk of Vijayapura district, Karnataka, India. Present study (2015) was also used to compare groundwater fluoride concentration in same 22 villages with previous government report (2000). Groundwater fluoride concentrations of 62 bore wells of 22 villages were analyzed by using an ion-sensitive electrode. A total of 660 adults and 600 children were screened for fluorosis symptoms and signs. Sixty clinically suspected fluorosis patients' urine samples were further analyzed for fluoride. The mean value (1.22 ± 0.75 mg/L) of fluoride concentration of 62 bore wells and 54.83 % bore wells with ≥1.0 mg/L of fluoride concentrations in Indi taluk indicates higher than the permissible limit of drinking water fluoride concentration recommended for India. Clinical symptoms like arthritis, joint pains, gastrointestinal discomfort and lower limb deformities with high urinary fluoride concentrations in some subjects suggest fluorosis. Results also showed an increase in groundwater fluoride concentration of the same 22 villages between previous and present study. Preliminary arthritis symptom of the villagers could be due to drinking fluoride-contaminated water. Increase in fluoride concentration with time to the bore wells definitely indicates future danger.

Asunto(s)

RESUMEN

BACKGROUND: Hattaraki pallye or prickly lettuce (Lactuca scariola Linn.) is one among several green leafy plants that grow in north Karnataka; it is usually consumed by the people of this region and is found to be antidiabetic in nature. The objective of this study is to evaluate hypoglycemic activities of supplementation with aqueous extract of prickly lettuce (L. scariola) leaves in vivo in acute and subchronic exposure with or without nickel (II) along with its glucose reduction capabilities with or without nickel (II) at pH 7.0 and 9.0 in vitro. METHODS: Percentage glucose reduction (in vitro) was determined by glucose oxidase-peroxidase enzymatic method at pH 7.0 and pH 9.0 using UV-Vis spectrophotometer. Hypoglycemic activities of L. scariola were carried out in alloxan-induced male diabetic rats at both acute and subchronic exposure. RESULTS: The results showed a significant alteration in the λmax value of Ni (II) in combination with L. scariola leaves extracts at both pH 7.0 and 9.0. The aqueous extract also produced a significant reduction in the glucose concentration at pH 7.0 and pH 9.0 even in presence of Ni (II) in vitro. Lactuca scariola leaves in either acute or subchronic supplementation showed a greater glucose tolerance and hypoglycemic regulation of blood sugar in diabetic rats with or without nickel (II) treatments. CONCLUSIONS: Lactuca scariola leaves can be a substitute for synthetic drugs to treat diabetic patients.

Asunto(s)

RESUMEN

BACKGROUND: Vitamin E is one of the important antioxidants linked to regulate various diseases, such as atherosclerosis, hypertension, and male infertility. A relatively simple and economic biochemical modified method has been developed to determine serum α-tocopherol concentration. METHODS: The current modified method is based on previous Baker and Frank method and the method of Martinek by using 2,2'-bipyridyl, ferric chloride, and xylene. The complex of ferrous ions generated in this reaction with 2,2'-bipyridyl is determined by using a plain enzyme-linked immunosorbent assay microplate (non-antibody coated) at 492 nm. RESULTS: The standard curve of this new modified method shows a linearity with correlation r=0.997 (concentration vs. absorbance). The absorbance of this color complex is directly proportional to the α-tocopherol concentration. The sensitivity of this new modified method has been compared and correlated with Baker and Frank method by using 15 human samples (r=0.99, p<0.0001). CONCLUSIONS: This simple and economic method may be routinely used to analyze α-tocopherol concentration in serum.

Asunto(s)

RESUMEN

OBJECTIVE: To evaluate the alteration of chemical behavior of L-ascorbic acid (vitamin C) with metal ion (nickel) at different pH solutions in vitro. METHODS: Spectra of pure aqueous solution of L-ascorbic acid (E mark) compound and NiSO4 (H2O) (sigma USA) were evaluated by UV visible spectrophotometer. Spectral analysis of L-ascorbic acid and nickel at various pH (2.0, 7.0, 7.4 and 8.6) at room temperature of 29 °C was recorded. In this special analysis, combined solution of L-ascorbic acid and nickel sulfate at different pH was also recorded. RESULTS: The result revealed that λmax (peak wavelength of spectra) of L-ascorbic acid at pH 2.0 was 289.0 nm whereas at neutral pH 7.0, λmax was 295.4 nm. In alkaline pH 8.6, λmax was 295.4 nm and at pH 7.4 the λmax of L-ascorbic acid remained the same as 295.4 nm. Nickel solution at acidic pH 2.0 was 394.5 nm, whereas at neutral pH 7.0 and pH 7.4 were the same as 394.5 nm. But at alkaline pH 8.6, λmax value of nickel sulfate became 392.0 nm. The combined solution of L-ascorbic acid and nickel sulfate (6 mg/mL each) at pH 2.0 showed 292.5 nm and 392.5 nm, respectively whereas at pH 7.0, L-ascorbic acid showed 296.5 nm and nickel sulfate showed 391.5 nm. At pH 7.4, L-ascorbic acid showed 297.0 nm and nickel sulfate showed 394.0 nm in the combined solution whereas at pH 8.6 (alkaline) L-ascorbic acid and nickel sulfate were showing 297.0 and 393.5 nm, respectively. CONCLUSIONS: Results clearly indicate an altered chemical behavior of L-ascorbic acid either alone or in combination with nickel sulfate in vitro at different pH. Perhaps oxidation of L-ascorbic acid to L-dehydro ascorbic acid via the free radical (HSc*) generation from the reaction of H2ASc + Ni (II) is the cause of such alteration of λmax value of L-ascorbic acid in the presence of metal nickel.

Asunto(s)

RESUMEN

Hexavalent chromium or chromium (VI) is a powerful epithelial irritant and a confirmed human carcinogen. This heavy metal is toxic to many plants, aquatic animals, and bacteria. Chromium (VI) which consists of 10%-15% total chromium usage, is principally used for metal plating (H2Cr2O7), as dyes, paint pigments, and leather tanning, etc. Industrial production of chromium (II) and (III) compounds are also available but in small amounts as compared to chromium (VI). Chromium (VI) can act as an oxidant directly on the skin surface or it can be absorbed through the skin, especially if the skin surface is damaged. The prooxidative effects of chromium (VI) inhibit antioxidant enzymes and deplete intracellular glutathione in living systems and act as hematotoxic, immunotoxic, hepatotoxic, pulmonary toxic, and nephrotoxic agents. In this review, we particularly address the hexavalent chromium-induced generation of reactive oxygen species and increased lipid peroxidation in humans and animals, and the possible role of garlic (Allium sativum Linn) as a protective antioxidant.

Asunto(s)

RESUMEN

We have studied the effect of simultaneous oral treatment of aqueous garlic extract (Allium sativum) on heavy metal (nickel II and chromium VI) induced changes in serum lipid profile. Nickel sulfate and potassium dichromate treated rats showed a significant increase in serum low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDL-C) and triglyceride (TG) level as well as decrease in serum high density lipoprotein-cholesterol (HDL-C) level. Simultaneous garlic administration with nickel sulfate showed improvement in serum LDL-C, HDL-C, VLDL-C and TG level. But in case of potassium dichromate, garlic administration did not show satisfactory improvement in lipid profile except VLDL-C and TG level. The results indicate that garlic (Allium sativum) has some beneficial effect in preventing heavy metal (nickel and chromium VI) induced alteration of lipid profile.

Asunto(s)

RESUMEN

In this experimental study, we investigated whether L-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO4). Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally L-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and L-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.

Asunto(s)

RESUMEN

We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.

Asunto(s)

RESUMEN

Nickel exposure greatly depletes intracellular ascorbate and alters ascorbate-cholesterol metabolism. We studied the effect of the simultaneous oral treatment with L-ascorbic acid (50 mg/100 g body weight (BW) and nickel sulfate (2.0 mg/100 g BW, i.p) on nickelinduced changes in serum lipid profiles and liver histopathology. Nickel-treated rats showed a significant increase in serum low-density lipoprotein-cholesterol, total cholesterol, triglycerides, and a significant decrease in serum high-density lipoprotein-cholesterol. In the liver, nickel sulfate caused a loss of normal architecture, fatty changes, extensive vacuolization in hepatocytes, eccentric nuclei, and Kupffer cell hypertrophy. Simultaneous administration of L-ascorbic acid with nickel sulfate improved both the lipid profile and liver impairments when compared with rats receiving nickel sulfate only. The results indicate that L-ascorbic acid is beneficial in preventing nickel-induced lipid alterations and hepatocellular damage.

Asunto(s)

RESUMEN

We studied the effect of oral treatment with ascorbic acid (50 mg/100 g body weight) on nickel sulfate-induced (2.0 mg/100 g body weight, i.p.) alteration of nucleic acids and total protein concentration in the liver of Wistar strain male albino rats. Nucleic acids and total protein concentrations in treated rats decreased significantly when compared with untreated controls. The simultaneous administration of ascorbic acid with nickel sulfate resulted in a remarkable improvement of nucleic acids and total protein concentrations in liver in comparison with rats treated with nickel sulfate only. The results indicate that nickel influences the expression of genetic information by reducing hepatic DNA, RNA, and protein concentration in animals. Simultaneous treatment with ascorbic acid was beneficial for fighting against nickel-induced hepatoxicity.

Asunto(s)