BackgroundMonosodium glutamate (MSG) is a widely-used flavor enhancer and stabilizer in ready-made or packaged foods. The excessive use of MSG has been shown to increase oxidative stress in different organ systems and causes glucose metabolism disorders, obesity, and coronary diseases.ObjectivesIn this study, the antioxidant activity of tannic acid was investigated experimentally with respect to its protective effects against overdosed MSG-induced oxidative stress in rats. The study took place in Turkey in August 2013.MethodsFour groups (n = 7) of three- to four-month-old Sprague-Dawley female rats were used in this study. The first group was the control, who were administered saline. The second group received tannic acid (50 mg/kg, 3 days) intraperitoneally (i.p.). The third group received MSG (2 g/kg, 7 days) i.p., and the fourth group received both tannic acid (50 mg/kg, 3 days, pretreatment) and MSG (2 g/kg, 7 days) i.p. The animals were euthanized ten days later. Blood was collected for determining the hematological values and blood glucose levels. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were determined in the brain, liver, and kidney homogenates, and in the erythrocyte hemolysate. Histopathological examination of the brain, liver, and kidneys was conducted through hematoxylin-eosin staining.ResultsThe data showed that the tannic acid treatment statistically decreased the MDA levels in the brain tissues of the group administered MSG and tannic acid (P < 0.001) when compared to the corresponding values of the control group. The SOD activities in the blood hemolysates of the MSG and tannic acid group increased when compared to the corresponding values for the MSG group (P < 0.01). Additionally, we found that pretreatment with tannic acid reduced blood glucose levels in comparison to the levels of the MSG group (P = 0.029). The results of our study show that tannic acid pretreatment in adult rats decreased blood glucose levels and oxidative stress.ConclusionsIn the literature, it was observed that short-term MSG exposure does not cause significant histological changes in the kidneys, liver, or brain cortex. These findings should be re-evaluated in additional long-term studies.
Cadmium (Cd) is among the heavy metals causing environmental pollution and can cause temporary or permanent oxidative stress in the cells. Antioxidative enzyme mechanisms may be inadequate in the response of living organisms to oxidative stress caused by these toxic substances. In this study, in order to prevent Cd induced oxidative stress, the possible protective effects of (TA), cacao oil (CO) and St. John's Wort oil (JWO) on lipid erythrocytes and antioxidant enzymes were investigated. We prepared packed erythrocytes from the blood samples of 7 healthy volunteers. Experiment groups consisting of control, Cd, TA, CO, JWO and their combinations (Cd+TA, Cd+CO ve Cd+JWO) were arranged. In all groups, malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were measured. Comparisons between groups of normally distributed variable were evaluated by One-Way variance analysis (ANOVA). Comparisons between groups of not normally distributed variable wereevaluated by Kruskal-Wallis test. After Cd administration SOD activity was increased in TA (3507± 68.2 u/gHb), CO (3518 ±170.0 u/gHb) and JWO (3469±249.5 u/ gHb) groups compared to Cd group. After Cd administration MDA levels were decreased in CO (52,1±24,3 nmol/gHb) and JWO (54,1±23,7 nmol/gHb) groups compared to Cd group. However, it did not change in the TA (61,5±50,0 nmol/gHb) group. After Cd administration CAT activity was increased in TA (228,2±31,3 u/gHb), CO (281,6±295,3 u/gHb) and JWO (267,8±69,4 u/gHb) groups compared to Cd group (196,2±223,0 u/gHb). These results indicate that HF and SCI may reduce Cd-induced oxidative stress, but TA is not very effective in terms of MDA levels. These data obtained in terms of other studies may be guiding.
Bu çalışmada Türk popülasyonunda nikotin kullanım bozukluğu (NUD) ile ilişkili olarak rs 221473, rs 221497, rs1004212 ve rs11624704 bölgelerindeki Neurexin 3 gen (NRXN3) polimorfizmlerinin incelenmesi amaçlanmıştır.Yöntem: Yapılan güç analizine göre nikotin kullanım bozukluğu ve kontrol grubunun 18-65 yaş arası 200'er kişiden oluşması kararlaştırıldı. Çalışma grubuna psikiyatrik bir birinci eksen bozukluğu, mental retardasyonu, geçirilmiş kafa travması veya herhangi bir nörolojik bozukluğu olmayan, en az 1 yıldır günde en az 10 sigara içen kişiler dahil edildi. Kontrol grubuna ise "hiç sigara içtiniz mi" sorusuna "hayır" cevabı veren ciddi kronik fiziksel bir hastalığı olmayan, daha önce geçirilmiş psikiyatrik bir bozukluğu ya da mental retardasyonu olmayan, sağlıklı gönüllü kişiler dâhil edildi. Tüm katılımcılara demografik verileri sorgulamayı içeren anket formu ve sigara kullananlara Fageström nikotin bağımlılık ölçeği uygulandı. Anketlerin uygulanmasını takiben DNA eldesi için katılımcılardan alınan venöz kan örneği, EDTA (etilen diamin tetra asetik asit) içeren tüplere alındı.Bulgular: Çalışmamızda seçilen dört gen bölgesinden rs11624704 için AC aleli taşıyan bireylerin, rs1004212için AG aleli taşıyan bireylerin sigara bağımlısı olma riskinin yüksek olduğu belirlenmiştir. Sonuç: Çalışmamız Türk örneklem grubunda NRXN3 ve nikotin kullanım bozukluğu ilişkisini araştıran ilk çalışmadır. Çalışmamızda Türk popülasyonunda nikotin kullanım bozukluğuna sahip olma riski ile Neurexin geninin ilişkili olabileceği gözlenmiştir.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.