Series-1 (Jul. – Aug. 2020)Jul. – Aug. 2020 Issue Statistics
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Abstract: Chronic intoxication of cyanide is known to produce some pathologic effects on different tissues, leading to alterations in biochemical parameters. Natural products, especially those derived from plants, have been used to help mankind sustain its health since the dawn of medicine. One such plant with extensive traditional use is Annona muricata. This study was aimed at determining the effects of ethyl acetate extract of Annona muricata leaves on cyanide (CN) induced tissue lesions in rabbits of the New Zealand strain. Four groups of rabbits,(5 per group) were used for the study. Group A(positive control), received pure grower's mash. Group B(negative control) receivedgrower's mash which had been compounded with 400mg CN/kg of feed. Group Creceived grower's mash.....
Key Words: Annona muricata, Ethyl acetate, Cyanide.
[1]. Ellenhorn, M. J. (1997). Cyanide poisoning. In: Ellenhorn's medical toxicology: diagnosis and treatment of human poisoning. Ellenhorn, M. J., Schonwald, S., Ordog, G., Wasserberger, J. (eds) Baltimore:Williams& Wilkins. Pp 1474–84.
[2]. Mathangi, D. C., Namasivayam, A. (2000). Effect of chronic cyanide intoxication on memory in albino rats. Food Chemistry and Toxicology .38:51–55.
[3]. Okolie, N. P., Iroanya, C. U. (2003). Some histologic and biochemical evidence for mitigation of cyanide-induced tissue lesions by antioxidant vitamin administration in rabbits. Food Chemistry and Toxicology.41:463–469.
[4]. Okolie, N. P., Asonye, C. C. (2004). Mitigation of cataractogenic potential of cyanide by antioxidant vitamin administration. Journal of Medicine and Biomedical Research.3:48–52.
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Abstract: Background: Breast cancer is a complex disease, constitutes a main community health concern. Mutation in tumor suppressors' genes and oncogenes were involved in its pathogenesis. Methylenetetrahydrofolate reductase helps in the 5, 10-methylenetetrahydrofolate transformation into 5-methyltetrahydrofolate. 5-methyltetrahydrofolate assists in the re-methylation of homocysteine to de novo methionine necessary for DNA production. In this study we analyze the relationship between the MTHFR gene C677T [rs1801133] polymorphism and the risk of breast cancer. Materials and Methods: This case–control study was carried out on 50 women with breast cancer and 50 women who apparently healthy. Real time polymerase chain reaction technique was used to detect MTHFR gene C677T [rs1801133] polymorphism.....
Key Words: Breast cancer, gene polymorphism, Methylenetetrahydrofolate reductase, real-time polymerase chain reaction.
[1]. Siegel RL, Miller KD, JamilA (2017): Cancer statistics, CA Cancer Journal for Clinicians; [67]: 7-30.
[2]. Motawi TM, Sadik NA, Shaker OG, et al. (2016): Study of microRNAs-21/221 as potential breast cancer biomarkers in Egyptian women. Gene; S0378-1119(16)00104-9.
[3]. Mancuso MR, Massarweh SA (2016): Endocrine therapy and strategies to overcome therapeutic resistance in breast cancer. Current problems in cancer PMID; 27839747.
[4]. Chon J, Stover PJ, Field MS (2017): Targeting nuclear thymidylate biosynthesis. Molecular Aspects of Medicine; 53: 48–56.
[5]. Elizabeth KE, Praveen SL, Preethi NR, et al. (2017): Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers. European Journal of Clinical Nutrition; 71[12]: 1437.
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Abstract: The ratio of the human population and the quantity of the eatable items are inversely proportional. The quantity of food items is decreased due to certain reasons such as, environmental conditions, unavailability of the water for farming, less income of farmers etc. The principal problem, concerning with GMO (Genetically Modified Organism) is the less information available in the public domain. Still the method for development of organism is bizarre for the public. Considering it, this compilation is aimed to sketch out the pitfalls for the implementation of GMO in the real world, and the advantages of GMO for the betterments of human society are listed. This overview will provide the detail information about the listed problems and shed off the myths and also open up the new paths to bring out the solution for the available problem in the area of genetically modified organism .
Key Words: GMO, GMO crops, Patenting of GMO, Pitfall of GMO.
[1]. Tencalla FG, Nickson TE, Garcia-Alonso M (2009). Environmental risk assessment.In: Environmental Impact of Genetically Modified Crops; Ferry N, Gatehouse AMR (ed): CAB International, Wallingford; 61-73. http://doi.org/10.1079/9781845934095.0000.
[2]. Seymour V (2016). The human- nature relationship and its impact on health: A critical review. Front. Public Health 4: 260. http://doi.org/10.3389/fpubh.2016.00260/
[3]. Wilkinson MJ, Sweet J, Poppy GM (2003). Risk assessment of GM plants, avoiding gridlock. Trends Plant Sci. 8: 208-212. https://doi.org/10.1016/S1360-1385(03)00057-8.
[4]. Verma C, Nanda S, Singh RK, Singh RB, Mishra S (2011). A review on impacts of genetically modified food on human health. The Open Nutraceuticals Journal 4: 3-11. http://doi.org/ 10.2174/1876396001104010003
[5]. Oliver MJ, Li Y (2013. Plant Gene Containment. Oliver MJ, Li Y (eds): Wiley-Blackwell Press, Iowa; 10.1002/9781118352670.
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Abstract: Background:Velvet beans (Mucunapruriens) is a tropical leguminous plant that belongs to Mucuna genus, the Fabaceae family. Various studies have reported the bioactivity of Mucunapruriens, such as increasing the sexual activity of normal male rats, hepatoprotective activity and its use in the treatment of diabetes and hypertension. Materials and Methods: In this study, its hepatoprotective ability was investigated in rats induced with NiCl2 toxicity. Alanine aminotransferase (ALT) activity, aspartate aminotransferase (AST) activity and arginase activity were determined in rats treated with aqueous extracts of Mucunapruriens (MPE). Lipid peroxidation was also determined by measuring malondialdehyde (MDA) levels in the liver homogenate of NiCl2-induced rats..... .
Key Words: Hepatoprotective, Lipid peroxidation,Quercetin,Mucunapruriens, Nickel chloride
[1]. Adjroud O The toxic effects of nickel chloride on liver, erythropoiesis, and development in Wistar albino preimplanted rats can be reversed with selenium pretreatment. Environ Toxicol. 2013;28(5):290-298.
[2]. Hfaiedh N, Allagui MS, Hfaiedh M, Feki AE, Zourgui L, Croute F. Protective effect of cactus (Opuntiaficusindica) cladode extract upon nickel-induced toxicity in rats. Food ChemToxicol. 2008;46(12):3759-3763. doi:10.1016/j.fct.2008.09.059
[3]. Chalasani NP, Hayashi PH, Bonkovsky HL, Navarro VJ, Lee WM, Fontana RJ. Practice Parameters Committee of the American College of Gastroenterology. ACG Clinical Guideline: the diagnosis and management of idiosyncratic drug-induced liver injury. Am. J. Gastroenterol. 2014;109(7):950-66; quiz 967.
[4]. +Duda-Chodak A, Baszczyk U. The impact of nickel on human health. Journal of Elementology, 2008;13:685–696.
[5]. Das KK, Buchner V. Effect of nickel exposure on peripheral tissues: role of oxidative stress in toxicity and possible protection by ascorbic acid. Reviews on Environmental Health. 2007; 22:157–173..
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Abstract: The andiroba (Carapa guianensis Aubl.) tree is a native Meliaceae family species from the Amazon region that has an important socioeconomic function due to its (wood / bark / leaf / seeds) several applications for the indigenous population. Its seed has one of the most healing oils known in that region. The andiroba oil (AO) applications vary from anti-living organisms (bacteria / fungi / insect / parasite) attack, to diseases (itching / fever / asthma / sore throat /wound) symptoms healing / cure. This review gathers literature information regarding AO characteristics related to tree and seed botany, oil extraction procedures, sensory specifics, physical and chemical composition, apart from its effects against different living organisms and their susceptibilities. Also, information regarding its health and food applications, including possible toxicity and seed residues utilization..
Key Words: Andiroba; Oil; Decontamination; Fungi; Food; Amazon
[1] Ambrozim ARP. (2000). Química e atividade inseticida do óleo de Carapa guianensis e das folhas de Canavaliaensiformis[Dissertação]: Universidade Federal de São Carlos;
[2] Ambrozin ARP, Leite AC, Bueno FC, Vieira PC, Fernandes JB, Bueno OC. (2006). Limonoids from andiroba oil and Cedrela fissilisand their insecticidal activity. Journal of the Brazilian Chemical Society.;17(3):542-7.
[3] Andrade EH, ZoghbiMdG, Maia JG. (2001). Volatiles from the leaves and flowers of Carapa guianensis Aubl. Journal of Essential Oil Research. 13:436-8.
[4] Andrade FFd. (2008). Desenvolvimento e avaliação de cristais líquidos obtidos em emulsões O/A a base de óleo de andiroba e ésterfosfórico [dissertation]. Ribeirão Preto: Universidade de São Paulo.
[5] Araújo, L. A. (2008). Estudo das Propriedades Físicas, Químicas e Termofísicas de Óleos Regionais e Suas Misturas (Doctoraldissertation, Tese. Universidade Federal do Pará. Brasil).
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Abstract: Alloxan, a derivative of urea is known to be a carcinogen and cytotoxic glucose analog. It is also known to be one of the most common diabetogenic agents to assay the antidiabetic efficacy of plant extracts and pure compounds in a number of diabetic animal models. In the present investigation the diabetogenic efficacy of different concentrations of alloxan has been assayed on albino mice. The results revealed that alloxan induced a multiphasic plasma glucose response when injected intraperitoneally in albino mice. 50 mg/kg BW and 100 mg/kg BW of alloxan did not cause a rise in plasma glucose level up to 50 hours. After 50 hours of exposure 50 mg/kg/W and 100 mg/kg BW cause a rise in the plasma glucose level to 115.2 mg/dL and 120.0 mg/dL respectively that was within the normal reference range. The hyperglycemic activity of albino mice increased on increasing......
Key Words: Alloxan, Albino Mice, Diabetogenic agent
[1]. Lenzen S (2008): The mechanisms of alloxan- and streptozotocin-induced diabetes. Diabetologia 51(2):216–26
[2]. Goldner MG, Gomori G (1944): Studies on the mechanism of alloxan diabetes. Endocrinology 35 (4):241–8.
[3]. Cruz AB, Amatuzio DS, Grande F, Hay LJ (1961): Effect of intra-arterial insulin on tissue cholesterol and fatty acids in alloxan-diabetic dogs. Circ Res, 9 (1):39–43.
[4]. Dunn JS, McLetchie NG (1943): Experimental alloxan diabetes in the rat. Lancet, 242(6265):384–7.
[5]. Gomori G, Goldner MG (1945): Acute nature of alloxan damage. Proc Soc Exp Biol Med 58 (3):232–3.