scholarly journals PROTECTIVE EFFECT OF CHLORELLA VULGARIS ON DNA DAMAGE, OXIDATIVE STRESS, AND LUNG MORPHOLOGICAL CHANGES IN CIGARETTE SMOKE-EXPOSED RATS

Author(s):  
Zamri Ks ◽  
Norripin Mkn ◽  
Darus Fi ◽  
Ekambaram Dg ◽  
Abdul Raof Nd ◽  
...  

Objective: The aim of this study was to determine the protective effect of Chlorella vulgaris (ChV), antioxidant-rich unicellular green alga, and in cigarette smoke-exposed rats.Methods: Male Sprague Dawley rats were divided into 4 groups: Control Group (C), ChV group (300 mg/kg body weight), cigarette smoke-exposed (S) group, and S group treated with ChV (S+ChV). Blood samples were drawn from the orbital sinus on days 0, 15, and 30 for the determination of DNA damage by Comet assay and plasma malondialdehyde (MDA) using high-performance liquid chromatography. Rats were killed on day 30, and lung tissue samples were taken for the evaluation of airspace enlargement and number of inflammatory cells.Results: Increased DNA damage (1004.8 au + 329.2, day 15; 1102.7 + 197.8, day 30) and high MDA levels (10.66 + 0.27, day 15; 10.29 + 0.9 day 30) were found in cigarette smoke-exposed rats on days 15 and 30 but were reduced significantly (p<0.05) when treated with ChV (DNA: 482.6 + 223.3, day15; 423.5 + 74.6, day 30 and MDA: 6.1 + 0.6, day15; 6.6 + 2.5, day 30) for both days. Hematoxylin and eosin staining showed that cigarette smoke-exposed rats had high frequency of airspace enlargement and number of inflammatory cells which were reduced when treated with ChV.Conclusion: ChV has a protective role in cigarette smoke-exposed rats by reducing oxidative DNA damage, MDA levels, lung cells inflammation, and airspace enlargement.

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Zhicheng Zhang ◽  
Haoran Kang

Abstract Background: The study was aimed to investigate the protective effect of Asarum sieboldii Miq. essential oil (AEO) on ovalbumin (OVA)-induced allergic rhinitis (AR) in rats. Methods and results: Sixty Sprague–Dawley male rats were randomly divided into six groups (n=10): control, model, cetirizine (Cet, 4.65 g/kg), and AEO (0.5, 1.5, 3 g/kg) groups. All animals except the control group received repeated intranasal instillation with 20 μl of 20% OVA in Al(OH)3 saline solvent for 15 days. The control group was intranasally instilled with 5 mg/ml of Al(OH)3 instead of the same procedure. In the 15 days, Cet and AEO were orally administrated for 28 days. At the end of the drug administration, 20 μl of 5% OVA was given to animals to stimulate allergic reaction, then the rat behavioral detection, assessment of the patho-morphological changes in nasal mucosa, and the serum biomarkers were determined. The result showed that AEO could significantly reduce the amount of nasal secretions, sneezing, and the degree of nasal scratching in AR rats with EC50 = 1.5 and 2.8 g/kg, respectively. The degree of nasal mucosal inflammation in AEO group improved, the levels of immunoglobulin E (IgE), histamine, IL-4, IL-5, IL-17 were decreased, and the level of IFN-γ was increased obviously with EC50 = 2 g/kg. Conclusion: The study suggested that the possible mechanism might be related with the inhibition of histamine release and regulation of the cytokine levels, which plays an important role in the treatment of AR.


2021 ◽  
Vol 13 (1) ◽  
pp. e843
Author(s):  
Fatma Sahindokuyucu-Kocasarı ◽  
Selinay Basak Erdemli-Kose ◽  
Zeki Erol ◽  
Simge Garlı

Objective. The aim of this study was to determine the protective effect of p-coumaric acid (p-CA) against toluene-induced hepatotoxicity, nephrotoxicity and neurotoxicity in rats. Materials and methods. A total of 32 Sprague-Dawley male rats, 8 in each group, were used. 4 groups were formed as control, toluene, p-CA and toluene+p-CA. Animals in the control group, toluene group and p-CA group were given 0.9% NaCl, 0.9 mg/kg b.w toluene and 100 mg/kg b.w p-CA orally for 21 days, respectively. The animals in toluene+p-CA group were received p-CA for 3 days and from day 4, toluene and p-CA were applied together daily until day 25. On the 25th day, the study was terminated, blood and tissue samples were collected. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine levels in serum, glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) and glutathione (GSH) levels in the tissue samples were determined. Results. In this study, it was determined that there were significant increases in ALT and AST activities, and creatinine levels in toluene-induced group compared to control group. Moreover, there was a decrease in the GSH-Px activities and GSH levels, and an increase in the MDA levels compared to the control group. However, in the toluene+p-CA group, significant decreases in aminotransferases activities, creatinine and MDA levels, and significant increases in GSH-Px activities and GSH levels were determined compared to the toluene group. Conclusions. It has been determined that p-CA has a protective effect against toluene-induced hepatotoxicity, nephrotoxicity and neurotoxicity.


2009 ◽  
Vol 29 (2) ◽  
pp. 93-101 ◽  
Author(s):  
Amal A El-Bakary ◽  
Sahar A El-Dakrory ◽  
Sohayla M Attalla ◽  
Nawal A Hasanein ◽  
Hala A Malek

Methanol poisoning is a hazardous intoxication characterized by visual impairment and formic acidemia. The therapy for methanol poisoning is alcohol dehydrogenase (ADH) inhibitors to prevent formate accumulation. Ranitidine has been considered to be an inhibitor of both gastric alcohol and hepatic aldehyde dehydrogenase enzymes. This study aimed at testing ranitidine as an antidote for methanol acute toxicity and comparing it with ethanol and 4-methyl pyrazole (4-MP). This study was conducted on 48 Sprague-Dawley rats, divided into 6 groups, with 8 rats in each group (one negative control group [C1], two positive control groups [C2, C3] and three test groups [1, 2 and 3]). C2, C3 and all test groups were exposed to nitrous oxide by inhalation, then, C3 group was given methanol (3 g/kg orally). The three test groups 1, 2 and 3 were given ethanol (0.5 g/kg orally), 4-MP (15 mg/kg intraperitoneally) and ranitidine (30 mg/kg intraperitoneally), respectively, 4 hours after giving methanol. Rats were sacrificed and heparinized, cardiac blood samples were collected for blood pH and bicarbonate. Non-heparinized blood samples were collected for formate levels by high performance liquid chromatography. Eye balls were enucleated for histological examination of the retina. Ranitidine corrected metabolic acidosis (p = .025), decreased formate levels (p = .014) and improved the histological findings in the retina induced by acute methanol toxicity.


2017 ◽  
Vol 9 (2) ◽  
pp. 196 ◽  
Author(s):  
Hamed R. Takruri ◽  
Maha S. Shomaf ◽  
Saida F. Shnaigat

This research was conducted to study the protective effect of bee honey on the 7,12-dimethylbenz(a)anthracene (DMBA)- induced breast cancer in rat model. The study consisted of three groups: honey group, positive control group (PC), and negative control group (NC) to which the carcinogen was not administered. All rats were fed the diet recommended by the American Institute of Nutrition for growing rats (AIN-93G), with addition of honey (50 g/kg diet) to the honey group. All Rats were fed their diets ad libitum on 12 hours dark/light cycle. At the age of 50 days all rats in the honey and PC groups were gavaged once by the carcinogen DMBA with a dose of 80 mg/kg body Wt. After three weeks of carcinogen administration, rats were palpated weekly to detect any tumor growth. After 18 weeks, all rats were sacrificed. The palpable structures and the mammary glands along with associated lymph nodes were removed and fixed in saline formalin and prepared for histopathological examination. The results revealed that the honey group diet significantly (p < 0.05) reduced the incidence rate of mammary cancer, palpable tumor multiplicity, tumor size and weight compared to the PC group. In conclusion, multi floral honey has a protective effect against DMBA- induced mammary cancer in the initiation, promotion, and progression stages of DMBA-induced mammary carcinogenesis. However, further research is needed to reveal the mechanisms that might have contributed to the preventive effect of honey against mammary cancer.


2011 ◽  
Vol 34 (3) ◽  
pp. 163 ◽  
Author(s):  
Omur Tabak ◽  
Remise Gelisgen ◽  
Hayriye Erman ◽  
Fusun Erdenen ◽  
Cüneyt Muderrisoglu ◽  
...  

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients.


2021 ◽  
Author(s):  
Atta Mohammad Dost ◽  
Mehmet Gunata ◽  
Onural Ozhan ◽  
Azibe Yildiz ◽  
Nigar Vardi ◽  
...  

Abstract Amikacin (AK) is frequently used in the treatment of gram-negative and some gram-positive infections. However, its use is limited due to nephrotoxicity due to the increase in reactive oxygen radicals. The aim of this study was to investigate the role of carvacrol (CAR) against AK-induced nephrotoxicity in rats. Thirty-two Sprague Dawley rats were randomly divided into four groups as control (Vehicle), AK (400 mg/kg), CAR + AK (80 mg/kg CAR + 400 mg/kg AK), and AK + CAR (400 mg/kg AK + 80 mg/kg CAR) groups. AK and CAR were administered via intramuscular and per-oral for 7 days, respectively. Blood and kidney tissue samples were taken at the end of the experiment. Renal function and histopathological changes were compared, and the relevant parameters of oxidative stress and inflammation were detected. Histopathological findings (necrotic changes and dilatation and inflammatory cell infiltration) significantly increased in the AK group compared to the control group. Also, the rats in the AK group lost weight significantly. It was found that CAR treatment before and after AK significantly improved nephrotoxicity histopathologically (p < 0.05). However, this improvement was not detected biochemically. These results show that CAR treatment before and after AK improves nephrotoxicity in the histopathological level.


2009 ◽  
Vol 296 (5) ◽  
pp. H1321-H1328 ◽  
Author(s):  
Zhenhua Wang ◽  
Ziyang Huang ◽  
Guorong Lu ◽  
Ling Lin ◽  
Markus Ferrari

Exposure to an adverse intrauterine environment increases the risk of cardiovascular disease later in adult life. However, the time course relationship between prenatal hypoxia and the onset of atherosclerosis in offspring remains unknown. The purpose of this study is to evaluate the role of reduced fetal oxygen supply on early development of atherogenesis in the adult offspring and further assess its susceptibility to sex-, hyperlipidemia-, and postnatal hypoxemia-related differences. Based on a 4 × 2 full factorial design consisting of four factors of maternal hypoxia, sex, hyperlipidemia, and postnatal hypoxemia, characteristics of growth were determined, and histopathological observation and morphometric analysis of the thoracic aortas were performed in Sprague-Dawley rat offspring. Intrauterine growth restriction, altered body shape at birth, and accelerated postnatal weight gain occurred in the maternal hypoxia group but did not occur in the control group. In 16-mo-old maternal hypoxia offspring, the thoracic aortas exhibited lesions similar to early events in atherosclerosis that involved impaired endothelial cells, thickening and fibration of intimas, infiltration of inflammatory cells to the subendothelial space, and migration and proliferation of vascular smooth muscle cells to the intima. In contrast, no detectable pathological changes were observed in the offspring without maternal hypoxia exposure. Morphometric analysis further demonstrated that prenatal hypoxia caused a significant thickening of intima ( P < 0.001) with a main effect of 5.5 μm, an approximately twofold increase compared with controls. In addition, there was a positive additive relationship between prenatal hypoxia and hyperlipidemia on the intimal thickness ( P < 0.05). There were no other main effects or interaction among these four factors. In summary, our results indicate that maternal hypoxia during pregnancy leads to early pathological appearances of atherogenesis in adult offspring. This effect was enhanced with hyperlipemia but was unaffected by postnatal hypoxia or sex.


2000 ◽  
Vol 20 (6) ◽  
pp. 699-702 ◽  
Author(s):  
Kyo-Cheol Mun ◽  
Mi-Young Yeo ◽  
Sang-Pyo Kim ◽  
Hyun-Chul Kim ◽  
Chun-Sik Kwak

Objective During peritoneal dialysis, the peritoneum is exposed to waste products, including urea. Urea forms cyanate spontaneously at body temperature and pH, and cyanate carbamylates amino acids, peptides, and proteins. Cyanate may contribute to peritoneal injury with morphological changes in the peritoneum. To test this hypothesis, we injected cyanate into rats. Methods Experiments were performed in two groups of 7 rats each. In the cyanate group, each rat received 1 mL of 1.5 μmol/L potassium cyanate dissolved in 40 mmol/L sodium bicarbonate solution intraperitoneally each experiment day. In the control group, each rat received 1 mL of 1.5 μmol/L potassium bicarbonate instead of potassium cyanate. The rats in both groups were anesthetized and killed at the 85th day after the first injection. After formalin fixation, tissue samples from abdominal walls and livers were sliced, embedded in a standard manner, and stained with hematoxylin and eosin. Results Parietal peritoneum from rats in the cyanate group showed a mild increase in the number of fibroblasts, with collagen deposits, infiltration by mononuclear cells, vascular congestion, round-shaped transformation of mesothelial cells, widening of submesothelial spaces, and abundant denudation of mesothelial cells. The visceral peritoneum from rats in the cyanate group showed collagen deposits with fibroblastic proliferation. Conclusions Cyanate can induce chronic inflammation in the peritoneum, and exposure of the peritoneum to cyanate may contribute to peritoneal injury in patients being treated with peritoneal dialysis.


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