Protective role of zinc in liver damage in experimental diabetes demonstrated via different biochemical parameters

Author(s):  
Ozlem Sacan ◽  
Ismet Burcu Turkyilmaz ◽  
Bertan Boran Bayrak ◽  
Ozgur Mutlu ◽  
Nuriye Akev ◽  
...  
Author(s):  
Divya Jyothi Palati ◽  
Swaroopa Rani Vanapatla

Objective: The present study was aimed to investigate the protective effect of methanolic extract of the whole plant of Aerva monsoniae (MEAM) and selenium on cadmium (Cd)-induced oxidative liver damage in experimental rats.Methods: In the present study, albino Wistar rats were treated with Cd (5 mg/kg), selenium (1 mg/kg), and MEAM (250 and 500 mg/kg) for 21days. After 21 days of the treatment, the rats were sacrificed, and blood was collected for estimation of biochemical parameters and liver was used for histopathological studies.Results: Oral administration of Cd significantly elevated the levels of hepatic markers such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, γ-glutamyl transferase, cholesterol, total bilirubin, direct bilirubin, and decreased levels of total proteins and albumin. We also observed that elevated oxidative stress markers such as malondialdehyde reduced the enzymatic antioxidants such as superoxide dismutase, catalase, and non-enzymatic antioxidants such as reduced glutathione in the liver. Co-administration of MEAM and selenium in Cd-intoxicated rats, the altered biochemical parameters, and pathological changes were recovered significantly (p>0.01) than the individual effects of MEAM and selenium.Conclusion: From the above findings, it was concluded that combination of MEAM and selenium exhibited remarkable protective effects against Cd-induced oxidative liver damage in rats.


2014 ◽  
Vol 66 (3) ◽  
pp. 1271-1279 ◽  
Author(s):  
Jelena Mladenovic ◽  
Milica Paunovic ◽  
Milos Matic ◽  
Veroljub Knezevic ◽  
Branka Ognjanovic ◽  
...  

The effects of subchronic exposure to copper (Cu) on lipid peroxidation, hemato-biochemical parameters, and the possible protective role of flavonoids Quercetin and (-)-Epicatechin were studied. Male Wistar albino rats were treated with Cu (560 mg/L, p.o. as CuCl2?2H2O for 5 weeks) and Quercetin and (-)-Epicatechin (40 mg/kg BW each, i.p., every third day during the last 3 weeks) alone or in combination. Cu increased the concentration of lipid peroxides, decreased the number of erythrocytes, hemoglobin and hematocrit values and increased the activities of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase. Coadministration of Quercetin and (-)-Epicatechin with Cu lowered the process of lipid peroxidation and restored examined hemato-biochemical parameters to control values. Our results indicate that Cu induced oxidative damage in erythrocytes, which led to anemia, while Quercetin and (-)-Epicatechin showed a protective effect on the hemato-biochemical processes in the blood of rats.


2007 ◽  
Vol 2007 ◽  
pp. 1-6 ◽  
Author(s):  
Nalan Kuzu ◽  
Kerem Metin ◽  
Adile Ferda Dagli ◽  
Fatih Akdemir ◽  
Cemal Orhan ◽  
...  

2009 ◽  
Vol 296 (6) ◽  
pp. G1318-G1323 ◽  
Author(s):  
Ping Yao ◽  
Liping Hao ◽  
Natascha Nussler ◽  
Antje Lehmann ◽  
Fangfang Song ◽  
...  

It has been reported that naturally occurring quercetin exerts hepatoprotective effects through heme oxygenase-1 (HO-1) induction. However, the precise mechanism of how ethanol-associated liver damage is counteracted by quercetin-enhanced HO-1 metabolism still remains unclear. To further decipher the protective role of quercetin on ethanol-induced liver damage, we treated human hepatocytes with quercetin and various (end) products of the HO-1 pathway. Our data clearly showed that quercetin treatment attenuated ethanol-induced damage, whereas hemoglobin and zinc protoporphyrin 9 (ZnPP) abolished such effects. Iron-II aggravated ethanol toxicity and was only partially reduced by quercetin. In contrast, carbon monoxide (CO) dose dependently inhibited ethanol-induced cytochrome P450 2E1 (CYP 2E1) activity and hepatotoxicity but had no influence on CYP 2E1 protein expression. Similarly, hemoglobin dramatically stimulated CYP 2E1 activity but not the protein expression in quercetin- and ethanol-cotreated hepatocytes. ZnPP significantly promoted CYP 2E1 protein expression in the presence and absence of CO treatment but inhibited ethanol-induced CYP 2E1 activation following CO incubation in quercetin- and ethanol-cotreated hepatocytes. These results suggested that quercetin virtually attenuated ethanol-derived oxidative damage via HO-1 induction. Heme degradation and CO release may mediate the protective effects through inhibiting ethanol-induced CYP 2E1 synthesis and enzymatic activity, respectively.


2014 ◽  
Vol 20 (30) ◽  
pp. 4828-4833 ◽  
Author(s):  
Cezary Chojnacki ◽  
Ewa Walecka-Kapica ◽  
Marek Romanowski ◽  
Jan Chojnacki ◽  
Grazyna Klupinska
Keyword(s):  

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