Resistance to oxidative stress by hyperplastic and neoplastic rat liver tissue monitored in terms of production of unpolar and medium polar carbonyls

1986 ◽  
Vol 883 (2) ◽  
pp. 207-214 ◽  
Author(s):  
G POLI ◽  
G CECCHINI ◽  
F BIASI ◽  
E CHIARPOTTO ◽  
R CANUTO ◽  
...  
2020 ◽  
Vol 1 (2) ◽  
pp. 43
Author(s):  
Andri Muhrim Siddiq ◽  
Muhammad In'am Ilmiawan ◽  
Mitra Handini

Background: The chemotherapeutic use of cisplatin (CP) is restricted because of its hepatotoxicity induced by oxidative stress. Malondialdehyde (MDA) is a secondary product of lipid peroxidation as a biomarker of oxidative stress. Individual administration of black seed oil (BSO) or honey (H) demonstrated hepatoprotective effect in rats. Interaction of both substances when administrated as combination can be evaluated using combination index (CI) to quantitatively depict synergism (CI<1), additive (CI=1) and antagonism effect (CI>1). Objective: to know the combination effect of BSO and honey on rat liver tissue given CP exposure. Methods: This study used 30 rats were divided into 10 groups. Normal group (N); Negative control group (NC); P1-P4 groups were administerated BSO (1 and 2 mL/kg) and honey (3.7 and 7.4 mL/kg); P5-P8 groups were combination of BSO and H. P1-P8 groups were given BSO and honey orally for 21 days. On the 18th day, NC and P1-P8 groups were given CP 8 mg/kg intraperitoneally, while the N group was given NaCl 0.9% 1 mL/kg intraperitoneally. Result: Malondialdehyde (MDA) levels were found to be lower in P1-P8 groups compared to negative control group and P6 and P7 groups have levels equivalent to MDA levels of normal control group (p > 0.05). Conclusion: Combination of BSO and honey provides a protective effect on cisplatin-induced rat liver tissue damage indicated by reduced MDA levels, but all combination group showed antagonism effect.


2021 ◽  
Author(s):  
Jagjeet Singh ◽  
Annu Phogat ◽  
Chandra Prakash ◽  
Vijay Kumar ◽  
Vinay Malik

Abstract The present study evaluated the effect of N-acetylcysteine (NAC) against sub chronic monocrotophos (MCP) exposure induced oxidative stress in rat liver. Albino wistar rats were divided into control, NAC treated, MCP and MCP treated groups. An oral dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) was administered for 28 days. We observed high oxidative stress generation on MCP exposure in liver tissue as evident by significant increase in lipid peroxidation, protein oxidation and decreased glutathione content followed by altered activities of superoxide dismutase, catalase and acetylcholinesterase. Sub chronic MCP exposure caused an array of cellular and structural alternations in lipids and proteins of liver tissue as depicted by the FTIR, histopathological and electron microscopic analysis. N-acetylcysteine attenuated the loss of glutathione and prevented lipid peroxidation and protein oxidation. Pre-treatment of NAC also restored histological and ultra space structural alternations. So NAC protects oxidative stress and tissue damage induced by sub chronic MCP exposure in rat liver; suggesting the therapeutic and antioxidant potential of NAC.


2018 ◽  
Vol 448 (1-2) ◽  
pp. 43-50 ◽  
Author(s):  
M. Stojanović ◽  
D. Todorović ◽  
Lj Šćepanović ◽  
D. Mitrović ◽  
S. Borozan ◽  
...  

Molecules ◽  
2011 ◽  
Vol 16 (11) ◽  
pp. 9116-9128 ◽  
Author(s):  
BoKang Cui ◽  
Su Liu ◽  
XiaoJun Lin ◽  
Jun Wang ◽  
ShuHong Li ◽  
...  

2021 ◽  
Vol 273 ◽  
pp. 02014
Author(s):  
Olga Pavlova ◽  
Olga Gulenko ◽  
Konstantin Krupin ◽  
Pavel Boriskin ◽  
Victor Leonov

The metabolic processes of the human body are based on multiple redox reactions and oxidative stress occurs when homeostasis is imbalanced. Antioxidant system of the body is represented by such enzymes as catalase, glutathione reductase, superoxidismutase and glutathione peroxidase. Objective: to study the dynamics of glutathione reductase activity in rat liver tissues after cryodestruction of right atrial myocardium to initiate oxidative stress. Materials and methods: 420 male rats were used. The rats were divided into two groups - intact and experimental, 210 animals in each. To initiate oxidative stress, the experimental group rats underwent cryodestruction of the right atrium. The activity of glutathione reductase in the liver tissue was determined by accumulation of oxidized glutathione before the experiment, as well as on 1, 3, 5, 7 and 14 days of the experiment. Conclusions: oxidative stress arising after cryodestruction of the right atrium up to the 7th day of the experiment provokes a decrease in the glutathione reductase activity in the rat liver tissue, but the start of reparative processes helps to restore the disturbed redox equilibrium in the body and normalize the enzyme level.


2020 ◽  
Vol 1 (2) ◽  
pp. 1
Author(s):  
Andri Muhrim Siddiq ◽  
Muhammad In'am Ilmiawan ◽  
Mitra Handini

Background: The chemotherapeutic use of cisplatin (CP) is restricted because of its hepatotoxicity induced by oxidative stress. Malondialdehyde (MDA) is a secondary product of lipid peroxidation as a biomarker of oxidative stress. Individual administration of black seed oil (BSO) or honey (H) demonstrated hepatoprotective effect in rats. Interaction of both substances when administrated as combination can be evaluated using combination index (CI) to quantitatively depict synergism (CI<1), additive (CI=1) and antagonism effect (CI>1). Objective: to know the combination effect of BSO and honey on rat liver tissue given CP exposure. Methods: This study used 30 rats were divided into 10 groups. Normal group (N); Negative control group (NC); P1-P4 groups were administerated BSO (1 and 2 mL/kg) and honey (3.7 and 7.4 mL/kg); P5-P8 groups were combination of BSO and H. P1-P8 groups were given BSO and honey orally for 21 days. On the 18th day, NC and P1-P8 groups were given CP 8 mg/kg intraperitoneally, while the N group was given NaCl 0.9% 1 mL/kg intraperitoneally. Result: Malondialdehyde (MDA) levels were found to be lower in P1-P8 groups compared to negative control group and P6 and P7 groups have levels equivalent to MDA levels of normal control group (p > 0.05). Conclusion: Combination of BSO and honey provides a protective effect on cisplatin-induced rat liver tissue damage indicated by reduced MDA levels, but all combination group showed antagonism effect.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 976
Author(s):  
Natalia N. Bezborodkina ◽  
Sergey V. Okovityi ◽  
Boris N. Kudryavtsev

Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.


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