Effect of perinatal biotin deficiency on auditory pathway of the Wistar-Albino rats

2019 ◽  
Vol 139 (8) ◽  
pp. 677-684
Author(s):  
Nevreste Didem Sonbay Yılmaz ◽  
Özer Erdem Gür ◽  
Nuray Ensari ◽  
Erdogan Bulut ◽  
Ozlem Tugce Kaya ◽  
...  
2020 ◽  
Vol 50 (6) ◽  
pp. 1580-1584
Author(s):  
Nevreste Didem SONBAY YILMAZ ◽  
Cem SAKA ◽  
Sibel ALİCURA TOKGÖZ ◽  
Murat ÇALIŞKAN ◽  
Erkan VURALKAN ◽  
...  

Background/aim: Ischemia is insufficient blood flow to provide adequate oxygenation. In the present study, we aimed to show whether acute hypoxia has a critical oxygen value that may lead to the deterioration of cochlear function.Materials and methods: Under general anesthesia, prehypoxic signal-to-noise ratios were determined by distortion product otoacoustic emissions (DPOAE). The oxygen saturation (SaO2) values of rats were monitored with an oxygen saturation probe. Rats were injected with an extra dose of anesthetic agent, and SaO2 was reduced. DPOAE values in SaO2 100–90, 90–80, 80–70, and 70–60 posthypoxic values were measured and compared statistically with prehypoxic values.Results: At 3000 and 4000 Hz, SaO2 70–60 values measured after the hypoxia were observed to be statistically significantly lower than the values measured before the hypoxia. At 6000 and 8000 Hz, SaO2 80–70 and 70–60 values measured after the hypoxia were observed to be statistically significantly lower than the values measured before the hypoxia. At 10,000 Hz, all of the values measured after the hypoxia were observed to be statistically significantly lower than the values obtained before the hypoxia.Conclusion: Many studies have been conducted on the effects of hypoxia on the inner ear. It remains unclear how fluctuations in DPOAE levels affect hearing in clinical trials when the SaO2 starts to decrease. Although hypoxia has been implicated in the etiology of sudden hearing loss and tinnitus, the effects of acute hypoxia on the cochlea are still uncertain. Further studies are needed on this subject.


Author(s):  
Pradeep Deshmukh ◽  
Tanaji Nandgude ◽  
Mahendra Singh Rathode ◽  
Anil Midha ◽  
Nitin Jaiswal

The suspensions of alcoholic extract of root bark of the plant Calotropis gigantea in 0.6% carboxy methyl cellulose (CMC) were evaluated for hepatoprotective activity in Wistar albino rats by inducing hepatic injury with D-galactosamine (400 mg/kg). Alcoholic extract of root bark of the plant Calotropis gigantea at an oral dose of 200 mg/kg and 400 mg/kg exhibited a significant (P<0.001, P<0.01 and P<0.05) protection effect by normalizing the levels of aspartate amino transferase (ASAT/ GOT), alanine amino transferase (ALAT/GPT), alkaline phosphatase (ALP), total bilirubin (TB), lactate dehydrogenase (LDH), which were significantly (P<0.001) increased in rats by treatment with 400 mg/kg i.p. of D-galactosamine. Silymarin (25 mg/kg), a known hepatoprotective drug used for comparison exhibited significant activity (P<0.001).


2020 ◽  
Vol 19 (2) ◽  
pp. 217-221
Author(s):  
Maria Jesús Lisbona-González ◽  
Candela Reyes-Botella ◽  
Esther Muñoz-Soto ◽  
Maria Victoria Olmedo-Gaya, ◽  
Jorge Moreno-Fernandez ◽  
...  

Adipose tissue is an endocrine organ and has central role in interaction with other organs or tissues while propolis can induce lipolysis. Therefore, the aim of this study is to provide detailed information about adipose tissue homeostasis modifications and body composition during propolis supplement consumption. Twenty male Wistar albino rats (8 weeks) were divided into two groups of 10 animals each and fed for 90 days with two different types of diets: standard for the control group (diet C) and standard diet + 2% propolis (diet P). Thyroid hormones did not show differences, while ghrelin and adiponectin decreased in the group that was fed propolis. Insulin, leptin, and non-esterified fatty acids also increased along with reduced body weight and fat, in addition to increased lean mass when propolis was in the diet. We conclude that propolis could decrease ghrelin and adiponectin but increase non-esterified fatty acids and insulin secretion, which improves body composition.


Author(s):  
Amin Al-Doaiss ◽  
Yazun Jarrar ◽  
Ali Shati ◽  
Mohammad Alfaifi ◽  
Mohammed Al-Kahtani ◽  
...  

Background: Atorvastatin (ATOR) is widely used for the treatment and prevention of hypercholesterolemia and various diseases, such as cardiovascular complication, with little data about the histopathological and ultrastructural renal alterations that might be induced by this drug. Objectives: The present study was undertaken to investigate the potential toxicity of therapeutic doses of atorvastatin on the microanatomy and ultrastructure of renal tissues from Wistar albino rats. Methods: Adult male Wistar albino rats received an oral daily dose of 5 mg/kg body weight for 90 consecutive days. Biopsies from both kidneys of each study rat were taken for histopathological and ultrastructural examination. Results: ATOR-treated rats exhibited glomerular, tubular, and interstitial histological alterations, including degeneration, necrosis, hyaline droplets, edema, cortical hemorrhages, mesangial hypercellularity, and blood capillary dilation and congestion. In addition, ATOR exposure increased the activity of glucose-6-phosphate dehydrogenase and alkaline phosphatase with a concurrent reduction in proteins and neutral mucosubstances content of the glomeruli and renal cells. Moreover, ATOR-treated animals demonstrated glomerular ultrastructural alterations, consisting mainly of capillary tuft dilatation, glomerular basement membrane thickening, and mesangial cell proliferation. The renal cells of the proximal tubules demonstrated damaged mitochondria, degenerative cellular changes, endoplasmic reticulum dilatation, lysosomal and autophagosome activation, nuclear alteration, myelin figure formation, and microvilli disorganization. Conclusion: The findings of the present work may indicate that ATOR can induce renal histological, histochemical, and ultrastructural alterations that may affect kidney and other vital organ function.


2017 ◽  
Vol 24 (1) ◽  
pp. 22 ◽  
Author(s):  
S. Priyanga ◽  
S. Hemmalakshmi ◽  
B. Vidya ◽  
P. Chella Perumal ◽  
V. K. Gopalakrishnan ◽  
...  

Author(s):  
Ayşe Esra Karadağ ◽  
Ayşegül Çaşkurlu ◽  
Mehmet Evren Okur ◽  
Etil Guzelmeric ◽  
Neslihan Üstündağ Okur ◽  
...  

2021 ◽  
pp. 096032712110036
Author(s):  
MC Üstüner ◽  
C Tanrikut ◽  
D Üstüner ◽  
UK Kolaç ◽  
Z Özdemir Köroğlu ◽  
...  

Carbon tetrachloride (CCl4) is a toxic chemical that causes liver injury. CCl4 triggers endoplasmic reticulum (ER) stress and unfolded protein response (UPR). UPR triggers autophagy to deal with the damage. The aim of this study was to investigate the effect of baicalein, derived from Scutellaria baicalensis, on CCl4-induced liver damage concerning ER stress and autophagy. Two groups of Wistar albino rats (n = 7/groups) were treated with 0.2 ml/kg CCl4 for 10 days with and without baicalein. Histological and transmission electron microscopy (TEM) analysis, autophagy, and ER stress markers measurements were carried out to evaluate the effect of baicalein. Histological examinations showed that baicalein reduced liver damage. TEM analysis indicated that baicalein inhibited ER stress and triggered autophagy. CCl4-induced elevation of C/EBP homologous protein (CHOP), glucose-regulating protein 78 (GRP78), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6), inositol requiring enzyme 1 (IRE1), pancreatic ER kinase (PERK), and active/spliced form of X-box-binding protein 1 (XBP1s) ER stress markers were decreased by baicalein. Baicalein also increased the autophagy-related 5 (ATG5), Beclin1, and Microtubule-associated protein 1A/1B-light chain 3-phosphatidylethanolamine-conjugated form (LC3-II) autophagy marker levels. In conclusion, baicalein reduced the CCl4-induced liver damage by inhibiting ER stress and the trigger of autophagy.


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