Hepatic morphological changes and oxidative stress in chronic streptozotocin-diabetic rats

Evelson, Pablo; Susemihl, C; Villarreal, I.; Llesuy, Susana; Rodríguez, Rosalía; Peredo, Horacio A.; Lemberg, A; Perazzo, Juan Carlos; Filinger, Ester Julia

doi:10.1016/s1665-2681(19)32074-5

Cited by 30 publications

(21 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[35] Liver tissue from the diabetic group did not show any evidence of the occurrence of ROS[35] and is consistent with our findings. Increased NO production in DM did not alter cellular function in liver tissue.…”

Section: Discussionsupporting

confidence: 90%

Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Vaghasiya

Sheth

Bhalodia

et al. 2010

Saudi J Gastroenterol

View full text Add to dashboard Cite

Background/Aim:This study was designed to investigate the possible effect of exenatide (Glucagon like Peptide-1 receptor agonist) on liver injury (distant organ) induced by renal ischemia reperfusion (IR) in diabetic rats.Materials and Methods:In vivo renal IR was performed in both type 2 diabetic and normal rats. Each protocol comprised ischemia for 30 minutes followed by reperfusion for 24 hours and a treatment period of 14 days before induction of ischemia.Results:Lipid peroxidation, xanthine oxidase activity, myeloperoxidase activity and nitric oxide level in liver tissue were significantly increased (P < 0.01, P < 0.001, P < 0.001, P < 0.05, respectively), after IR in diabetic rats compared to normal rats. Antioxidant enzymes like glutathione, superoxide dismutase, catalase and glutathione peroxidase were significantly reduced (P < 0.05, P < 0.05, P < 0.01, P < 0.05, respectively), after IR in diabetic rats compared to normal rats. Exenatide treatment significantly normalized (P < 0.01), these biochemical parameters in treated rats compared to diabetic IR rats. Serum creatinine phosphokinase activity and liver function enzymes were also significantly normalized (P < 0.001, P < 0.001, respectively), after administration of exenatide.Conclusion:Exenatide exerted protective effect on exaggerated remote organ (liver) injury induced by renal IR in diabetes.

show abstract

Section: Discussionsupporting

confidence: 90%

Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Vaghasiya

Sheth

Bhalodia

et al. 2010

Saudi J Gastroenterol

View full text Add to dashboard Cite

show abstract

“…On the other hand, DM did not alter ROS production in liver tissue and these data are in good agreement with the work of Evelson et al (2005). Their results showed that livers from the diabetic group did not show evidence of the occurrence of ROS.…”

Section: Discussionsupporting

confidence: 88%

“…However, we found high NO level after DM. Evelson et al (2005) found that dilation of hepatic sinusoids and it was significantly different from control group. This increased NO production in DM did not alter cellular function in liver tissue as indicated in the present study.…”

Section: Discussionmentioning

confidence: 81%

Melatonin treatment against remote organ injury induced by renal ischemia reperfusion injury in diabetes mellitus

et al. 2008

View full text Add to dashboard Cite

Oxidative stress may have a role in liver damage after acute renal injury due to various reasons such as ischemia reperfusion (IR). Diabetes mellitus (DM) is an important disease for kidneys and may cause nephropathy as a long term complication. The aim of this study was to investigate protective effect of melatonin, a potent antioxidant, against distant organ injury on liver induced by renal IR in rats with or without DM. The rats were divided into six groups: control (n=7), DM (n=5), IR (n=7), DM+IR (n=7), melatonin+IR (Mel+IR) (melatonin, 4 mg/ kg during 15 days) (n=7), and Mel+DM+IR groups (n=7). Diabetes developed 3 days after single i.p. dose of 45 mg/kg streptozotocin. After 15 day, the left renal artery was occluded for 30 min followed 24 h of reperfusion in IR performed groups. DM did not alter oxidative parameters alone in liver tissue. The levels of malondialdehyde, protein carbonyl and nitric oxide with activities of xanthine oxidase and myeloperoxidase were increased in liver tissues of diabetic and non-diabetic IR groups. Nitric oxide level in DM was higher than control. The activities of catalase and superoxide dismutase were increased in IR groups in comparison with control and DM. ALT and AST levels were higher in IR and DM+IR groups than control and DM. Melatonin treatment reversed all these oxidant and antioxidant parameters to control values as well as serum liver enzymes. We concluded that renal IR may affect distant organs such as liver and oxidative stress may play role on this injury, but DM has not an effect on kidney induced distant organ injury via oxidant stress. Also, it was concluded that melatonin treatment may prevent liver oxidant stress induced by distant injury of kidney IR.

show abstract

“…Consequently, oxidative damages and liver and kidney tissue injuries leading to failure and dysfunctions were observed [35,36]. Elevated levels of liver enzymes, such as transaminases (AST and ALT), GGT, and LDH enzymes were, therefore, detected in the blood of diabetic rats [37,38].…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus plantarum TN627 significantly reduces complications of alloxan-induced diabetes in rats

et al. 2013

View full text Add to dashboard Cite

Hepatic morphological changes and oxidative stress in chronic streptozotocin-diabetic rats

Cited by 30 publications

References 25 publications

Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Melatonin treatment against remote organ injury induced by renal ischemia reperfusion injury in diabetes mellitus

Lactobacillus plantarum TN627 significantly reduces complications of alloxan-induced diabetes in rats

Contact Info

Product

Resources

About