Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 202
  • Home
  • Print this page
  • Email this page

 Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 14  |  Issue : 2  |  Page : 120-125

Effect of ethanolic extract of Ocimum gratissimum on sodium nitrite-induced cerebellar cortex toxicity in adult Wistar rats


Department of Human Anatomy, Faculty of Medicine, Ahmadu Bello University, Zaria, Kaduna State, 81006, Nigeria

Date of Web Publication19-Feb-2016

Correspondence Address:
Augustine Oseloka Ibegbu
Department of Human Anatomy, Faculty of Medicine, Ahmadu Bello University, Zaria, Kaduna State, 81006
Nigeria
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1596-2393.177022

Rights and Permissions
  Abstract 


Introduction: Intoxication of nitrites mainly from food and water constitute a potential hazard with a resultant hypoxia. Aim: The aim was to study the effects of ethanolic leaves extract of Ocimum gratissimum on sodium nitrite (NaNO2)-induced cerebellar toxicity in adult Wistar rats. Materials and Methods: Twenty-four adult Wistar rats weighing 150–250g were divided into six groups of four rats each. Group I was the control and received distilled water, Group II received 54 mg/kg body weight (bwt) of NaNO2, Group III received 750 mg/kg bwt of the extract and 54 mg/kg bwt of NaNO2, Group IV received 375 mg/kg bwt of the extract and 54 g/kg bwt of NaNO2, Group V received 54 mg/kg bwt of NaNO2and 2 ml/kg bwt of olive oil, and Group VI received 2 ml/kg bwt of olive oil. The administration was by oral route and lasted for 21 days, after which the animals were sacrificed and blood collected for analyses, and the tissues were processed for histological studies. Results: The result showed a decrease in the mean bwt of the animals in Groups III and IV, a significant increase in serum levels of malondialdehyde and a decrease in superoxide dismutase, glutathione peroxidase, and catalase in Group II. The result of the hematological analysis showed a significant increase in red blood cells, white blood cells, mean corpuscular volume, and mean corpuscular hemoglobin (P < 0.05). The result of histological studies showed degenerative changes in Group IIwith less degeneration in Group IV. Conclusion: The result showed that O. gratissimum in a controlled manner may be useful in the management of neurodegenerative conditions that involve free radical generation and reduction in brain energy production.

Keywords: Cerebellum free radical, enzymes, hypoxia, oxidative stress, Ocimum gratissimum


How to cite this article:
Ibegbu AO, Eze SM, Livinus PP, Adamu SA, Hamman OW, Umana UE, Musa SA. Effect of ethanolic extract of Ocimum gratissimum on sodium nitrite-induced cerebellar cortex toxicity in adult Wistar rats. J Exp Clin Anat 2015;14:120-5

How to cite this URL:
Ibegbu AO, Eze SM, Livinus PP, Adamu SA, Hamman OW, Umana UE, Musa SA. Effect of ethanolic extract of Ocimum gratissimum on sodium nitrite-induced cerebellar cortex toxicity in adult Wistar rats. J Exp Clin Anat [serial online] 2015 [cited 2019 Nov 12];14:120-5. Available from: http://www.jecajournal.org/text.asp?2015/14/2/120/177022




  Introduction Top


Reactive oxygen species (ROS) including free radicals such as superoxide anion (O ), hydroxyl (HO), hydrogen peroxide (H2O2), and peroxyl radicals (RCOO ) are active oxygen components that are by-product of normal body metabolism (Halliwell and Gutteridge, 2007). ROS are highly reactive and short-lived and are known to cause damage to cellular components including lipid, deoxyribonucleic acid, protein, carbohydrate, and other biological molecules. They consequently lead to many pathological processes such as cancer, cardiovascular diseases, diabetes, inflammation, and neurodegenerative diseases (Marouf, et al., 2010).

Several free radical species are generated during the course of nitrite-induced oxidation of hemoglobin (Hb) (Fan and Steinberg, 1996). Under normal physiologic conditions, aerobic metabolism of glucose is the primary metabolic fuel for energy production in the brain (Lowry, et al., 1964; Greene, et al., 2003). Although the brain represents only 2% of the body weight (bwt), it receives 15% of the cardiac output and consumes 20% of the total body oxygen (Magistretti and Pellerin, 1996). Many of the most common disorders of the brain, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple system disorder, progressive supranuclear palsy, and mitochondrial encephalomyopathy, have been found to be associated with alterations in cerebral oxygen metabolism (Ishii, et al., 1996). The brain is particularly vulnerable to the effects of ROS due to its high demand for oxygen and its abundance of highly peroxidisable substrates.

Sodium nitrite (NaNO2) is a chemical with a variety of applications. On its own, it can be toxic to humans, but when integrated into specific processes such as the preservation and curing of food, it can be a safeguard from much more dangerous bacteria that can grow in the food. NaNO2 are in many types of fertilizers, pesticides, herbicides, fabrics and have some applications in medicine. NaNO2 poses health risk on exposure. It is irritant to the eye, lungs, and skin and is toxic when consumed. It is not often handled outside professional settings because of its toxicity in high concentrations (Abramov, et al., 2003; Abdullahi, et al., 2012). NaNO2 oxidizes Hb to methemoglobins which contain ferric iron (Fe 3+) rather than ferrous iron (Fe 2+) present in Hb. Ferric ions have slightly greater affinity for O 2 which shift the oxygen dissociation curve to the left resulting in decrease release of O2 to the tissue (Patel and Chu, 2011). Acute intoxication is manifested primarily by methemoglobin formation and resultant hypoxia (Calabrese, et al., 1983; Hajieva and Behl, 2006). Nitrites, ingested from food mainly from cured meats and water supply, constitute a potential toxicity. Nitrites and nitrates have also been shown to react with various amines and amides to form carcinogenic nitroso compounds (Stoewsand, et al., 1973). Much attention has been focused on the use of antioxidants, especially natural antioxidants, for the improvement of human health (Zheng and Wang, 2001; Cristiana, et al., 2006).

Herbs have been used safely and effectively for many centuries and are free of most of the side effects associated with synthetic drugs (Njoku, et al., 1997; Murray, 2004). Ocimum gratissimum belongs to the family Lamiaceae and found mostly in the tropical countries. It is traditionally used to relief pains and also used in the treatment of rheumatism, diarrhea, high fever, convulsions, diabetes, eczema, and piles and as a repellant (Chitwood, 2003; Hotlets, et al., 2003; Pessoa, et al., 2002). The present work was aimed at studying the effects of ethanolic leaves extract of O. gratissimum against NaNO2 induced toxicity in adult Wistar rats.


  Materials and Methods Top


Experimental Protocol

Twenty-four apparently healthy adult Wistar rats of both sexes weighing between 150 and 250 g were purchased from the Department of Human Anatomy, Faculty of Medicine, Ahmadu Bello University, Zaria, Kaduna State. The animals were acclimatized for 3 weeks in the Department Animal House. The animals were fed with standard pellet and water ad libitum throughout the experimental period under controlled environment of 12 h cycle of light and dark cycle at room temperature. The rats were divided into six groups of four rats each. Fresh leaves of O. gratissimum were purchased from Sabon Gari Market Zaria, Kaduna State-Nigeria. Identification and authentication were carried out at the herbarium section of the Department of Biological Sciences, Ahmadu Bello University, Zaria, with voucher number 285.

The leaves were washed, rinsed with distilled water and, air-dried for the period of 1 week was extracted in the Department of Pharmacognosy, Faculty of Pharmaceutical Sciences, Ahmadu Bello University, Zaria. The dried fresh leaves of O. gratissimum were grounded into coarse powder of 500 g. The powder was subjected to absolute ethanol extraction using soxhlet apparatus for 10 h. The extract was concentrated by using an evaporating dish and was slowly evaporated to dryness in a Water bath regulated at 6°C, and 10% w/w dark green color of the extract was obtained.

Chemicals and Reagents

Twelve grams of NaNO2 manufactured by May and Bakers Limited, Dagenham, England, was purchased from Steve Moore Chemicals Limited, Samaru, Zaria-Nigeria. Goya olive oil was purchased from Beautiful Gate Pharmaceutical Limited, Samaru, Zaria-Kaduna State, Nigeria. Growers feed from Vital feed was obtained from Samaru Market Zaria, Kaduna, Nigeria, and was used to feed the animals throughout the experimental period.

Experimental Procedure

The dose of the extract was determined using the LD50 of 2500 mg/kg bwt (Rabelo, et al., 2003). The stock solution was prepared by dissolving 12 g of the extract in 160 ml of olive oil to form the stock solution; 30% (750 mg/kg bwt) and 15% (375 mg/kg bwt) of the LD50 were used in this study for the high and low dose, respectively. The animals were randomly divided into six groups of four animals per group. Group I received 2 ml/kg bwt of distilled water, Group II received 54 mg/kg bwt of NaNO2, Group III received 750 mg/kg bwt of the extract + 54 mg/kg bwt of NaNO2, Group IV received 375 mg/kg bwt of the extract + 54 g/kg bwt of NaNO2, Group V received 54 mg/kg bwt of NaNO2 + 2 ml/kg bwt of olive oil, and Group VI received 2 ml/kg bwt of olive oil. The experimental procedure was approved by the Ethics Committee of the Faculty of Veterinary Medicine, Ahmadu Bello University, Zaria.

Animal Sacrifice

After the last day of administration, the animals were left for 48 h and were fasted overnight before sacrificed. The animals were humanely sacrificed by cervical dislocation and the blood collected through cardiac puncture for hematological analysis, and some blood were centrifuged at 2500 rpm and serum collected for biochemical analysis.

Incision was made through the midsagittal suture, and the brains were removed and fixed in Bouin's fluid. The tissues were processed, sectioned, and stained with hematoxylin and eosin method and Cresyl fast violet method.

Estimation of Oxidative Parameters

Determination of catalase activity

Catalase (CAT) activity was determined using the method described by Sinha (1972), and the absorbance was read at 570 nm. Standard cure was made by plotting the absorbance obtained at various levels of the assay. The CAT activity was obtained from the graph of the standard curve.

Determination of superoxide dismutase activity

Superoxide dismutase (SOD) activity was determined by a method described by Fridovich (1989). Absorbance was measured every 30 s up for a total of 150 s at 480 nm from where the SOD activity was calculated.

Assessment of Lipid Peroxidation

Lipid peroxidation as evidenced by the formation of TBARS was measured by the method of Niehaus and Samuelson (1968). The absorbance of the pink supernatant was measured against a reference blank using a spectrophotometer at 535 nm.

Assay of Reduced Glutathione Concentration

Reduced glutathione (GSH) concentration measurements were done according to the method of Ellman (1959) as described by Rajagopalan, et al. (2004), and the absorbance was read at 412 nm.

Statistical Analysis

Data were reported as mean ± standard error of mean. One-way analysis of variance and Duncan's Multiple range test were used to compare the means with values of P < 0.05 was considered to be statistically significant. Sigmastat version 2.0 (Systat Inc., Point Richmond, CA) was used for the statistical analysis.


  Result Top


Physical Observations

Some physical observations were made during the period of administration. The animals in Group II were observed to be weak and breathe faster when compared to the control and Group VI. The animals in Groups III and IV were observed to feed well and drank a lot of water when compared to the animals in the control. The animals in the control and in Group VI showed increased activities in their locomotion and feeding habit to be normal.

Weight Changes

The mean bwt of animals in the control and Groups II, V, and VI were observed to increase during the period of administration while the animals in Group VI showed a more rapid increase in weight when compared with others. The mean change in weight in all the groups did not show statistical significance. Meanwhile, the animals in Group III showed a significance decrease in the mean final bwt when compared with the initial bwt as shown in [Table 1].
Table 1: Morphometric parameters cerebella, initial and final body weight (g)

Click here to view


Oxidative Enzymes

The effect on the level of oxidative enzymes such as SOD, malondialdehyde (MDA), glutathione peroxidase (GPX), and CAT showed no statistically significant difference in the parameters. The mean SOD of Group II showed significant decrease when compared to the control. There was significance increase in the mean MDA in Group II when compared to the control. The mean GPX in Groups II, III, V, and VI showed significant decrease when compared to the control. The mean CAT in Groups II, IV, V, and VI were observed decrease when compared to the control as shown in [Table 2].
Table 2: Oxidative parameters

Click here to view


Hematological Parameters

The mean value of pack cell volume (PCV), red blood cell count (RBC), Hb count, white blood cell count (WBC), mean corpuscular volume, mean corpuscular Hb (MCH), and MCH concentration of the experimental animals were studied. The result showed no statistically significant differences in the mean PCV across the groups. The mean WBC of the treated animals were statistically significanct (P ≤ 0.05) when compared to the control. The mean WBC of the animals in Groups II, V, and VI showed significant increase when compared with the Control. The mean Hb of the treated animals did not show any statistically significant difference when compared with the control. The result of the mean RBC of the treated groups showed statistically significant difference (P ≤ 0.05) when compared with the control [Table 3].
Table 3: Hematological parameters

Click here to view


Histological Observation

The result of histological observation of the sections of the cerebellar cortex of the animals showed some histological changes in the rats administered with NaNO2 with or without the extract and olive oil. The control showed normal architecture and orientation of the molecular layer, granular layer, and Purkinje layer with normal Purkinje cells of the cerebellar cortex as shown [Plate 1]. Group II showed some degeneration of the Purkinje cell layer and Purkinje cells of the cerebellar cortex as shown in [Plate 2]. Group III showed degeneration of the Purkinje cells in the cerebellar cortex as shown in [Plate 3]. Group IV animals showed mild degeneration Purkinje cell along with the Purkinje cell layer of the cerebellar cortex as shown in [Plate 4]. Group V showed the molecular layer and granular layer, Purkinje cell along with the Purkinje cell layer as shown in [Plate 5]. Whereas animals in Group VI showed normal orientation of the molecular layer, granular layer, and Purkinje layer with normal Purkinje cells of the cerebellar cortex as shown in [Plate 6].














  Discussion Top


The decrease in physical activities observed in experimental animals could be a result of reduced energy generation due to hypoxia resulting from methemoglobin formation. This may also be due to the increased level of NaNO2 in the body leading to increased catabolic process in the body. The results of this study are in agreement with Grant and Butler (1989) who reported that NaNO2 reduce energy generation due to hypoxia-induced methemoglobin formation. Porter, et al. (1993) had shown that NaNO2 increases the rate of catabolic reaction thus leading to the decrease in the mean bwt observed in Groups III and IV could be due to the hypoglycemic and diuretic effect of the extract. The present result is in agreement with the findings of Effraim, et al. (2003), which showed that the aqueous and ethanol extracts of O. gratissimum leaves possessed hypoglycemic effects on normoglycemic and neonatal streptozocin-induced diabetes model. The rats treated with NaNO2 showed significant decrease in mean bwt when compared the control throughout the experiment periods, and this reduction in weight may be due to the reduction in food consumption (Grant and Butler, 1989; Patel and Chu, 2011).

The chemical reactivity of NaNO2 with Hb may enhance iron-mediated toxicities. Nitrite is known to cause free radical generation (Rahman, et al. 2009; Zaidi, 2010), as it can stimulate oxidation of ferrous ions in oxy-Hb to form methemoglobin (Gladwin, 2004; Baky, 2010). The result of the present study showed that NaNO2 significantly impaired the oxidative status in the animals. This effect was shown by the significant increase in brain malondialdehyde, an index of lipid peroxidation in Group II animals and a significant reduction in the levels of GPX, in addition to decrease in SOD and CAT activities when compared with the control. The present result is in agreement with Hayashi, et al. (2004) and Valko, et al. (2006), which showed that there was a significant increase in the mean SOD, GPX, CAT and a decrease in the mean MDA. This could be as a result of ameliorative effect of O. gratissimum extract. The present result agrees with the findings of Fagbohun, et al. (2012) and Akinmoladun, et al. (2007) which showed that the leaf extract of O. gratissimum possesses antioxidant potential presumablybecause of the phytochemical constituents.

The cerebellum of animals in Groups II and III showed some degenerating cells with degeneration of the Purkinje cell layer and Purkinje cells of the cerebellar cortex. This could be due to methemoglobin formation due to nitrite ingestion and increase in concentration of nitrite and extract which could be toxic. The present result was in agreement with Imaizumi, et al. (1980) and Porter, et al. (1993) who showed that nitrite convert Hb to methemoglobin and Orafidiya, et al. (200l) had reported that O. gratissimum leaves have toxic potentials that should not be overlooked. Group IV treated with low dose of extract showed mild degeneration of cells which could be as a result of the antioxidant effect of the extract. This result is in agreement with Akinmoladun, et al. (2007) who reported that O. gratissimum possess good antioxidant properties due to its phytochemical constituents. Meanwhile, Group V showed more cytoarchitectural damage when compared with Group IV while the animals in the control and Group VI showed normal cytoarchitecture of the cerebral and cerebellar cortex.


  Conclusion Top


Administration of O. gratissimum leaves extract have shown to significantly protect the brain against oxidative stress-induced tissue damage and ameliorates the energy failure in damaged brain tissues induced by NaNO2. The current study greatly recommends the beneficial use of O. gratissimum in a dose-controlled manner in the management of neurodegenerative conditions that involve free radical generation and reduction in brain energy production, particularly in hypoxic states.[39]

Financial Support and Sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.

 
  References Top

1.
Abdullahi S., Umana U.E., Timbuak J.A., Hamman O.W., Musa S.A., Ikyembe D.T. (2012). Effect of aqueous and ethanolic extracts of Ocimum gratissimum on the histology of the spleen, haematological indices of wistar rats and its antimicrobial properties. Asian J Med Sci 4 (4):130-3.  Back to cited text no. 1
    
2.
Abramov A.Y., Canevari L., Duchen M.R. (2003). Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity. J Neurosci 23 (12):5088-95.  Back to cited text no. 2
    
3.
Akinmoladun A.C., Ibukun E.O., Emmanuel A., Obuotor E.M., Farombi E.O. (2007). Phytochemical constituent and antioxidant activity of extract from the leaves of Ocimum gratissimum. Sci Res Essay 2:163-6.  Back to cited text no. 3
    
4.
Baky N.A., Zaidi Z.F., Fatani A.J., Sayed-Ahmed M.M., Yaqub H. (2010). Nitric oxide pros and cons: The role of l-arginine, a nitric oxide precursor and idebenone, a coenzyme-Q analogue in ameliorating cerebral hypoxia in rat. Brain Res Bull 83 (1-2):49-56.  Back to cited text no. 4
    
5.
Calabrese E.J., Moore G.S., McCarthy M.S. (1983). The effect of ascorbic acid on nitrite-induced methemoglobin formation in rats, sheep, and normal human erythrocytes. Regul Toxicol Pharmacol 3 (3):184-8.  Back to cited text no. 5
    
6.
Chitwood D.J. (2003). Phytochemical based strategies for nematode control. Ann Rev Phytopathol 40:221-49.  Back to cited text no. 6
    
7.
Cristiana M., Murbach F., M'arcia O.M., Mirtes C. (2006). Effects of seasonal variation on the central nervous system activity of Ocimumgratissimum L. essential oil. J Ethnopharmacol 105 (1-2):161-6.  Back to cited text no. 7
    
8.
Effraim K.D., Jacks T.W., Sodipo O.A. (2003). Histopathological studies on the toxicity of Ocimum gratissimum Leaf extract on some organs of rabbit. Afr J Biomed Res 6 (1):21-5.  Back to cited text no. 8
    
9.
Ellman G.L. (1959). Tissue sulfhydryl groups. Arch Biochem Biophys 82 (1):70-7.  Back to cited text no. 9
    
10.
Fagbohun E.D., Lawal O.U., Orez M.E. (2012). The proximate, mineral and phytochemical analysis of the leaves of Ocimum gratissimum L. Melanthera scandens A. and Leea guineensis L. and their medicinal value. Int J Appl Biol Pharm Technol 3:0976-4550.  Back to cited text no. 10
    
11.
Fan A.M., Steinberg V.E. (1996). Health implications of nitrate and nitrite in drinking water: An update on methemoglobinemia occurrence and reproductive and developmental toxicity. Regul Toxicol Pharmacol 23 (1):35-43.  Back to cited text no. 11
    
12.
Fridovich I. (1989). Superoxide dismutase J Biol Chem 264:7761-4.  Back to cited text no. 12
    
13.
Gladwin M.T., Crawford J.H., Patel R.P. (2004). The biochemistry of nitric oxide, nitrite, and hemoglobin: Role in blood flow regulation. Free Radic Biol Med 36 (6):707-17.  Back to cited text no. 13
    
14.
Grant D., Butler W.H. (1989). Chronic toxicity of sodium nitrite in male F344 rat. Food Chem Toxicol 27 (9):565-71.  Back to cited text no. 14
    
15.
Greene S.A., Orova M.T., Seyfried T.N. (2003). Perspectives on the metabolic management of epilepsy through dietary reduction of glucose and elevation of ketone bodies. J Neurochem 86 (3):529-37.  Back to cited text no. 15
    
16.
Hajieva P., Behl C. (2006). Antioxidants as a potential therapy against age-related neurodegenerative diseases: Amyloid Beta toxicity and Alzheimer's disease. Curr Pharm Des 12 (6):699-704.  Back to cited text no. 16
    
17.
Halliwell B., Gutteridge J.M., editors. (2007). Free Radicals in Biology and Medicine. 4th ed. Oxford University Press, New York, USA, p. 617-783.  Back to cited text no. 17
    
18.
Hayashi T., Saito A., Okuno S., Ferrand-Drake M., Dodd R.L., Chan P.H. (2004). Oxidative injury to the endoplasmic reticulum in mouse brains after transient focal ischemia. Neurobiol Dis 15 (2):229-39.  Back to cited text no. 18
    
19.
Hotlets F.B., Ueda-Nakamura T., Cortez D.A., Morgado-Diaz J.A., Nakamura C.V. (2003). Effects of essential oil of Ocimum gratissimum on the trypanosomatid Herpetomonas Samuel Pessoa. Act Protozool 42:269-76.  Back to cited text no. 19
    
20.
Imaizumi K., Tyuma I., Imai K., Kosaka H., Ueda Y. (1980).In vivo Studies on Methemoglobin formation by sodium nitrite. Int Arch Occup Environ Health 45 (2):97-104.  Back to cited text no. 20
    
21.
Ishii K., Kitagaki H., Kono M., Mori E. (1996). Decreased medial temporal oxygen metabolism in Alzheimer's disease shown by PET. J Nucl Med 37 (7):1159-65.  Back to cited text no. 21
    
22.
Lowry O.H., Passonneau J.V., Hasselberger F.X., Schulz D.W. (1964). Effect of ischemia on known substrates and cofactors of the glycolytic pathway in brain. J Biol Chem 239:18-30.  Back to cited text no. 22
    
23.
Magistretti PJ., Pellerin L. (1996). Cellular mechanisms of brain energy metabolism. Relevance to functional brain imaging and to neurodegenerative disorders. Ann N Y Acad Sci 777:380-7.  Back to cited text no. 23
    
24.
Marouf B.H., Aziz T.A., Zalzala M.H. (2010). Free radical scavenging activity of Benfotiamine in nitrite-induced hemoglobin oxidation and membrane fragility models. J Pharm Biomed Sci 1:13-8.  Back to cited text no. 24
    
25.
Murray M.T. (2004). The Healing Power of Herbs. 2nd ed. Gramercy Books, New York.  Back to cited text no. 25
    
26.
Niehaus W.G., Samuelson B. (1968). Formation of malondialdehyde from phospholipids arachidonate during microsomal lipidperoxidation. Eur J Biochem 6 (1):126-30.  Back to cited text no. 26
    
27.
Njoku C.J., Zeng L., Asuzu I.U., Oberlies N.H., Mclaughlin J.L. (1997). Oleanolic acid, a bioactive component of the leaves of Ocimum gratissimum (Lamiaceae). Int J Pharm 35:134-7.  Back to cited text no. 27
    
28.
Orafidiya L.O., Ovadele A.O., Shittu A.O., Elujoba A.A. (2001). The formulation of an effective topical antibacterial product containing Ocimum gratissimum leaf essential oil. Int J Pharm 224 (1-2):177-83.  Back to cited text no. 28
    
29.
Patel V.P., Chu C.T. (2011). Nuclear transport, oxidative stress, and neurodegeneration. Int J Clin Exp Pathol 4 (3):215-29.  Back to cited text no. 29
    
30.
Pessoa L.M., Morais S.M., Bevilaqua C.M., Luciano J.H. (2002). Antihelminthic activity of essential oils of Ocium gratissium Linn. and eugonol activity against Haemoachus contortus. Vet Parasitol 109 (1-2):59-63.  Back to cited text no. 30
    
31.
Porter W.P., Green S.M., Dabbink N.L. (1993). Intractive effects of low concentration of carbamates aldicarb and methomyl and the triazine metribuzin of thyroxine and somatotropin levels in white rats. J Toxicol Environ Health 40 (1):15-34.  Back to cited text no. 31
    
32.
Rabelo M., Souza E.P., Soares P.M. (2003). Antinociceptive properties of the essential oil of Ocimum gratissimum L. (Labiatae) in mice. Braz J Med Biol Res 36 (4):521-4.  Back to cited text no. 32
    
33.
Rahman M.M., Kim S.J., Kim G.B., Hong C.U., Lee Y.U., Kim S.Z. et al. (2009). Nitrite induced methemoglobinaemia affects blood ionized and total magnesium level by hydrolysis of plasma adenosine triphosphate in rat. Basic Clin Pharmacol Toxicol 105 (5):294-300.  Back to cited text no. 33
    
34.
Rajagopalan R., Kode A., Penumatha S.V., Kallikat N.R., Venugopal P.M. (2004). Comparative effects of curcumin and an analog of curcumin on alcohol and PUFA induced oxidative stress. J Pharm Pharm Sci 83:2747-52.  Back to cited text no. 34
    
35.
Sinha A.K. (1972). Colorimetric assay of catalase. Anal Brochem 47 (2):389-94.  Back to cited text no. 35
    
36.
Stoewsand G.S., Anderson J.L., Gacia G.Y. (1973). Nitrite-induced methemoglobinemia in Guinea pigs: Influence of diets containing beets with varying amounts of nitrate, and the effect of ascorbic acid and methionine. J Nutr103 (3):419-24.  Back to cited text no. 36
    
37.
Valko M., Rhodes C.J., Moncol J., Izakovic M., Mazur M. (2006). Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact 160 (1):1-40.  Back to cited text no. 37
    
38.
Zaidi Z.F. (2010). Effects of sodium nitrite-induced hypoxia on cerebellar Purkinje cells in adult rats. Pak J Med Sci 26:2.  Back to cited text no. 38
    
39.
Zheng W., Wang S.Y. (2001). Antioxidant activity and phenolic compounds in selected herbs. J Agric Food Chem 49 (11):5165-70.  Back to cited text no. 39
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and Me...
Result
Discussion
Conclusion
References
Article Tables

 Article Access Statistics
    Viewed1603    
    Printed48    
    Emailed0    
    PDF Downloaded166    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]