Erythrocyte osmotic fragility and lipid peroxidation in experimental hyperthyroidism

Endocrine ◽  
2009 ◽  
Vol 36 (3) ◽  
pp. 498-502 ◽  
Author(s):  
Rıfat Yücel ◽  
Semra Özdemir ◽  
Nuran Darıyerli ◽  
Selmin Toplan ◽  
M. Can Akyolcu ◽  
...  
2019 ◽  
Vol 89 (3-4) ◽  
pp. 152-160
Author(s):  
Parisa Hasanein ◽  
Peyman Mohammadi-Raighan ◽  
Alireza Komaki

Abstract. Oxidative stress is part of the mechanisms involved in ethanol toxicity. We investigated effects of vitamins C (VC), E (VE) and the combination of VC+VE on chronic ethanol-induced toxicity in rat erythrocytes. The following groups were treated for 30 days: control (C), VC (200 mg/kg), VE (200 mg/kg), VC (200 mg/kg) + VE (200 mg/kg), ethanol 4 g/kg, ethanol + VC, ethanol + VE and ethanol + VC + VE. The doses of vitamins and ethanol were selected for per kilogram of animal’s body weight. Blood samples collected at the end of treatments were analyzed for erythrocyte osmotic fragility and plasma scavenging activity. The washed erythrocytes were used to determine superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdeyde (MDA). Ethanol induced erythrocyte fragility (p < 0.001) and increased lipid peroxidation (p < 0.001) in rat erythrocytes. Furthermore, there were significant decreases in plasma scavenging (p < 0.001), SOD (p < 0.001), CAT (p < 0.01) and GPx (p < 0.001) activities in erythrocytes of ethanol-treated animals. Although VC or VE alone restored all of ethanol-induced disturbances to near normal (p > 0.05) but there were still significant differences compared to control animals. Combination therapy completely corrected ethanol-induced erythrocyte fragility, lipid peroxidation and prooxidant/antioxidant imbalance. We showed the beneficial effects of VC and VE combination in decreasing erythrocyte fragility and lipid peroxidation in both ethanol and control groups. Therefore this combination treatment may provide a new potential alternative for prevention of ethanol toxicity which deserves consideration and further examination.


2017 ◽  
Vol 07 (03) ◽  
pp. 71-85 ◽  
Author(s):  
Ejike Daniel Eze ◽  
Yusuf Tanko ◽  
Ahmed Abubakar ◽  
Sheu Oluwadare Sulaiman ◽  
Karimah Mohammed Rabiu ◽  
...  

2021 ◽  
Vol 22 (14) ◽  
pp. 7307
Author(s):  
Ilya S. Zhukov ◽  
Larisa G. Kubarskaya ◽  
Inessa V. Karpova ◽  
Anastasia N. Vaganova ◽  
Marina N. Karpenko ◽  
...  

Trace amine-associated receptors (TAARs) are a group of G protein-coupled receptors that are expressed in the olfactory epithelium, central nervous system, and periphery. TAAR family generally consists of nine types of receptors (TAAR1-9), which can detect biogenic amines. During the last 5 years, the TAAR5 receptor became one of the most intriguing receptors in this subfamily. Recent studies revealed that TAAR5 is involved not only in sensing socially relevant odors but also in the regulation of dopamine and serotonin transmission, emotional regulation, and adult neurogenesis by providing significant input from the olfactory system to the limbic brain areas. Such results indicate that future antagonistic TAAR5-based therapies may have high pharmacological potential in the field of neuropsychiatric disorders. TAAR5 is known to be expressed in leucocytes as well. To evaluate potential hematological side effects of such future treatments we analyzed several hematological parameters in mice lacking TAAR5. In these mutants, we observed minor but significant changes in the osmotic fragility test of erythrocytes and hematocrit levels. At the same time, analysis of other parameters including complete blood count and reticulocyte levels showed no significant alterations in TAAR5 knockout mice. Thus, TAAR5 gene knockout leads to minor negative changes in the erythropoiesis or eryptosis processes, and further research in that field is needed. The impact of TAAR5 deficiency on other hematological parameters seems minimal. Such negative, albeit minor, effects of TAAR5 deficiency should be taken into account during future TAAR5-based therapy development.


2014 ◽  
Vol 43 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Victor Olusegun Sinkalu ◽  
Joseph Olusegun Ayo ◽  
Ariyo Adelaja Abimbola ◽  
Josiah Egbamushe Ibrahim

2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.


2016 ◽  
Vol 12 ◽  
pp. 82-84 ◽  
Author(s):  
Francesco Fazio ◽  
Stefania Casella ◽  
Claudia Giannetto ◽  
Elisabetta Giudice ◽  
Giuseppe Piccione

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