Antioxidant compound (E)-2-benzylidene-4-phenyl-1,3-diselenole protects rats against thioacetamide-induced acute hepatotoxicity

2017 ◽  
Vol 95 (9) ◽  
pp. 1039-1045
Author(s):  
Angélica S. Reis ◽  
Mikaela P. Pinz ◽  
Cristiani F. Bortolatto ◽  
Cristiano R. Jesse ◽  
Lucielli Savegnago ◽  
...  

The aim of this study was to investigate whether (E)-2-benzylidene-4-phenyl-1,3-diselenole (BPD) protects against hepatotoxicity induced by thioacetamide (TAA). On the first day of treatment, male adult Wistar rats received BPD (10 or 50 mg·kg–1). On the second day, the rats received a single intraperitoneal injection of TAA (400 mg·kg–1). Twenty-four hours after TAA administration, biochemical determinations and liver histological analysis were carried out. BPD (50 mg·kg–1) reduced plasma aspartate and alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities increased by TAA exposure. Treatment with BPD was effective against increased lipid peroxidation levels and attenuated a decrease in hepatic reduced glutathione and ascorbic acid levels as well as an inhibition of glutathione peroxidase activity caused by TAA exposure. The higher dose of BPD protected against the inhibition of hepatic δ-aminolevulinic dehydratase activity induced by TAA. Finally, histopathological examination of the liver showed that BPD markedly ameliorated TAA-induced hepatic injury. In conclusion, BPD protected against hepatotoxicity and oxidative stress caused by TAA exposure in rats.

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
António Nogueira ◽  
Francisco Peixoto ◽  
Maria Manuel Oliveira ◽  
Carlos André Pires ◽  
Bruno Colaço ◽  
...  

Purpose.This study aimed to evaluate the effect of chronic treatment with chaetomellic acid A (CAA) on oxidative stress and renal function in a model of renal mass reduction.Methods. Male Wistar rats were subjected to 5/6 nephrectomy (RMR) or sham-operated (SO). One week after surgery, rats have been divided into four experimental groups: RMR: RMR rats without treatment(n=14); RMR + CAA: RMR rats treated with CAA(n=13); SO: SO rats without treatment(n=13); and SO + CAA: SO rats treated with CAA(n=13). CAA was intraperitoneally administered in a dose of 0.23 µg/Kg three times a week for six months.Results.RMR was accompanied by a significant reduction in catalase and glutathione reductase (GR) activity(p<0.05)and a decrease in reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio. CAA administration significantly increased catalase and GR activity(p<0.05)and increased GSH/GSSG ratio, but no significant difference between the treated and nontreated groups was found in this ratio. No significant differences were found between the RMR groups in any of the parameters of renal function. However, CAA administration slightly improves some parameters of renal function.Conclusions.These data suggest that CAA could attenuate 5/6 RMR-induced oxidative stress.


2020 ◽  
Vol 8 (1) ◽  
pp. 6-17
Author(s):  
O.O. Adewale ◽  
K.H. Aremu ◽  
A.T. Adeyemo

Objective: Potential combined nephrotoxic effect following simultaneous administration of two food additives: potassium bromate (PBR) (20 mg/kg of body weight, twice weekly) and sodium nitrite (SNT) (60mg/kg of body weight as a single dose) orally was investigated. Methods: Nephrotoxicity was assessed by determining urea, creatinine and electrolyte concentrations in the serum. In addition, concentrations of nitric oxide, reduced glutathione, total thiol, malondialdehyde and activities of arginase, adenosine deaminase, catalase, superoxide dismutase, and glutathione perioxidase in the kidney were investigated. Results: The results revealed that individual exposure to PBR or SNT significantly induced nephrotoxicity and oxidative stress in rats however, this was enhanced by co-exposure as evidenced by significant alteration in these kidney markers when compared with the control. Conclusion: This study accentuates the risk of enhanced nephrotoxicity in food containing both additives. Key words: Potassium bromate, sodium nitrite, renal markers.


2008 ◽  
Vol 24 (10) ◽  
pp. 635-642 ◽  
Author(s):  
TS Shanmugarajan ◽  
D Sivaraman ◽  
I Somasundaram ◽  
M Arunsundar ◽  
E Krishnakumar ◽  
...  

D-Galactosamine (GalN)-induced liver injury is associated with reactive oxygen species and oxidative stress. In the present study, we evaluated the effect of alpha lipoic acid (ALA) supplementation on acute GalN-induced oxidative liver injury. Hepatotoxicity induced by single intraperitoneal injection of GalN (500 mg/kg body wt) was evident from increase in lipid peroxidation and serum marker enzymes (asparate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase). The decreased activities of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) as well as glutathione levels were the salient features observed in GalN-induced hepatotoxicity. Pretreatment with ALA (50 mg/kg body weight for 7 days) significantly precluded these changes and prevents the hepatic injury. Hence, this study clearly exemplified that ALA might be a suitable candidate against GalN-induced cellular abnormalities.


Author(s):  
Afolabi C. Akinmoladun ◽  
M. Tolulope Olaleye ◽  
Kayode Komolafe ◽  
Abayomi O. Adetuyi ◽  
Afolabi A. Akindahunsi

AbstractNovel hepatoprotectives are needed to address the increasing cases of liver problems worldwide.Adult male albino rats were divided into nine groups. Seven groups were pretreated with PE (50-, 100-, and 150 mg/kg), HP (25-, 50-, and 75 mg/kg) or silymarin (25 mg/kg), respectively, once daily for 5 consecutive days and then administered acetaminophen (2 g/kg) on the 5th day. The control and acetaminophen-intoxicated groups received normal saline throughout the experimental period, with the latter group additionally receiving 2 g/kg acetaminophen on the 5th day. Administrations were performed po.In the acetaminophen-intoxicated group, there were significant increases (p<0.05) in serum activities of alanine aminotransferase (31.72±3.3 vs. 22.1±1.2 U/I), aspartate aminotransferase (185.1±10.1 vs. 103.83±13.3 U/I), bilirubin level and hepatic malondialdehyde (2.32±0.3 vs. 1.42±0.1 units/mg protein), accompanied with significant decreases (p<0.05) in hepatic reduced glutathione level (0.10±0.01 vs. 0.23±0.03 units/mg protein) and glutathione peroxidase activity (2.51±0.2 vs. 3.25±0.2 μmol HPE and HP ameliorated most of the observed biochemical alterations with HP appearing to show more potency. The results suggest that the flavonoid, homopterocarpin contributes to the hepatoprotective and antioxidant potentials of


2019 ◽  
Vol 17 (4) ◽  
pp. 426-431
Author(s):  
Jin Xuezhu ◽  
Li Jitong ◽  
Nie Leigang ◽  
Xue Junlai

The main purpose of this study is to investigate the role of citrus leaf extract in carbon tetrachloride-induced hepatic injury and its potential molecular mechanism. Carbon tetrachloride was used to construct hepatic injury animal model. To this end, rats were randomly divided into 4 groups: control, carbon tetrachloride-treated, and two carbon tetrachloride + citrus leaf extract-treated groups. The results show that citrus leaf extract treatment significantly reversed the effects of carbon tetrachloride on the body weight changes and liver index. Besides, treatment with citrus leaf extract also reduced the levels of serum liver enzymes and oxidative stress in a dose-dependent manner. H&E staining and western blotting suggested that citrus leaf extract could repair liver histological damage by regulating AMPK and Nrf-2.


2019 ◽  
Vol 18 (4) ◽  
pp. 297-302
Author(s):  
Sriset Yollada ◽  
Chatuphonprasert Waranya ◽  
Jarukamjorn Kanokwan

Bergenin is a C-glucoside derivative of gallic acid but its antioxidant and hepatoprotective effects have not previously been compared with gallic acid. Male ICR mice were administered bergenin (10, 50, and 250 mg/kg/day) or gallic acid (100 mg/kg/day) for 7 consecutive days before a single administration of ethanol (5 g/kg). Liver sections were histopathologically examined. Aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde levels were determined in plasma. Total glutathione, reduced glutathione, and oxidized glutathione levels were determined in liver homogenates. Ethanol induced hepatic injury with prominent histopathological markers including nuclear pyknosis and necrotic areas and this accorded with increases in the plasma levels of aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde. Moreover, ethanol disturbed hepatic glutathione homeostasis by reducing glutathione stores. Hepatic injury in the ethanol-induced mice was prevented with bergenin and gallic acid by significant decreases in plasma aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde levels and restoration of the hepatic glutathione profile through an increase in the reduced glutathione/oxidized glutathione ratio. Bergenin at 10 mg/kg/day showed comparable hepatoprotective activity to gallic acid in an ethanol-induced mouse model of oxidative stress. Therefore, bergenin might be a promising candidate for further development as a novel hepatoprotective product.


1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.


Author(s):  
Olugbemi T. Olaniyan ◽  
Olakunle A. Ojewale ◽  
Ayobami Dare ◽  
Olufemi Adebayo ◽  
Joseph E. Enyojo ◽  
...  

Abstract Objectives Lead primarily affects male reproductive functions via hormonal imbalance and morphological damage to the testicular tissue with significant alteration in sperm profile and oxidative markers. Though, different studies have reported that Cocos nucifera L. oil has a wide range of biological effects, this study aimed at investigating the effect of Cocos nucifera L. oil on lead acetate-induced reproductive toxicity in male Wistar rats. Methods Twenty (20) sexually matured male Wistar rats (55–65 days) were randomly distributed into four groups (n=5). Group I (negative control)—distilled water orally for 56 days, Group II (positive control)—5 mg/kg bwt lead acetate intraperitoneally (i.p.) for 14 days, Group III—6.7 mL/kg bwt Cocos nucifera L. oil orally for 56 days and Group IV—lead acetate intraperitoneally (i.p.) for 14 days and Cocos nucifera L. oil for orally for 56 days. Rats were sacrificed by diethyl ether, after which the serum, testis and epididymis were collected and used for semen analysis, biochemical and histological analysis. Results The lead acetate significantly increases (p<0.05) testicular and epididymal malondialdehyde (MDA) levels, while a significant reduction (p<0.05) in sperm parameters, organ weight, testosterone and luteinizing hormone was observed when compared with the negative control. The coadministration of Cocos nucifera oil with lead acetate significantly increases (p<0.05) testosterone, luteinizing hormone, sperm parameters and organ weight, with a significant decrease (p<0.05) in MDA levels compared with positive control. Histological analysis showed that lead acetate distorts testicular cytoarchitecture and germ cell integrity while this was normalized in the cotreated group. Conclusions Cocos nucifera oil attenuates the deleterious effects of lead acetate in male Wistar rats, which could be attributed to its polyphenol content and antioxidant properties.


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