2007•PubMedRequires access

[A diabetic model for liver oxidant damage in mice].

Jiao, B Wang, Huang Cy, Shan Yu, Yin Wy

Open publisher page 1 citations

Abstract

OBJECTIVE: To observe the liver oxidant damage for diabetic model in mice. METHODS: Male kunming mice were feed with high fat dietary for a week and then were randomly divided into two groups by weight, with 10 mice in each group. One group was induced by small dose streptozotocin (STZ) and obtained STZ-induced diabetic mice, and the other group was regarded as the control. Both of the two groups were feed with high fat dietary. After 6 weeks, the activities of enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. Glutathione (GSH), maleic dialdehyde (MDA), nitric oxide (NO) levels in the liver and the liver viscera quotient were also measured. Liver histological manifestations were observed. RESULTS: In diabetes group, there was a significant decrease in body weight, and the activities of GSH, CAT, and NOS decreased significantly (t value were 5.370, 10.639, 5.235, 3.089, respectively, P < 0.01). While, the liver viscera quotient, the levels of MDA, GSH-PX and NO increased remarkably (t value were -6.246, -2.728, -2.660, -4.924, respectively, P < 0.01 or P < 0.05). The significant difference was not observed in SOD between the two groups (t value was -0.405, P > 0.05). The liver histological damages were observed in diabetes group, light microscope observation showed hepatocytes swelling, ballooned changing and fatty droplets clustering. CONCLUSION: The oxidant damage might exist in the liver diabetic model in mice.

About this research paper

What this paper is about

OBJECTIVE: To observe the liver oxidant damage for diabetic model in mice. METHODS: Male kunming mice were feed with high fat dietary for a week and then were randomly divided into two groups by weight, with 10 mice in each group. One group was induced by small dose streptozotocin (STZ) and obtained STZ-induced diabetic mice, and the other group was regarded as the control. Both of the two groups were feed with high fat dietary. After 6 weeks, the activities of enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. Glutathione (GSH), maleic dialdehyde (MDA), nitric oxide (NO) levels in the liver and the liver viscera quotient were also measured. Liver histological manifestations were observed. RESULTS: In diabetes group, there was a significant decrease in body weight, and the activities of GSH, CAT, and NOS decreased significantly (t value were 5.370, 10.639, 5.235, 3.089, respectively, P < 0.01). While, the liver viscera quotient, the levels of MDA, GSH-PX and NO increased remarkably (t value were -6.246, -2.728, -2.660, -4.924, respectively, P < 0.01 or P < 0.05). The significant difference was not observed in SOD between the two groups (t value was -0.405, P > 0.05). The liver histological damages were observed in diabetes group, light microscope observation showed hepatocytes swelling, ballooned changing and fatty droplets clustering. CONCLUSION: The oxidant damage might exist in the liver diabetic model in mice.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVE: To observe the liver oxidant damage for diabetic model in mice. METHODS: Male kunming mice were feed with high fat dietary for a week and then were randomly divided into two groups by weight, with 10 mice in each group. One group was induced by small dose streptozotocin (STZ) and obtained STZ-induced diabetic mice, and the other group was regarded as the control. Both of the two groups were feed with high fat dietary. After 6 weeks, the activities of enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. Glutathione (GSH), maleic dialdehyde (MDA), nitric oxide (NO) levels in the liver and the liver viscera quotient were also measured. Liver histological manifestations were observed. RESULTS: In diabetes group, there was a significant decrease in body weight, and the activities of GSH, CAT, and NOS decreased significantly (t value were 5.370, 10.639, 5.235, 3.089, respectively, P < 0.01). While, the liver viscera quotient, the levels of MDA, GSH-PX and NO increased remarkably (t value were -6.246, -2.728, -2.660, -4.924, respectively, P < 0.01 or P < 0.05). The significant difference was not observed in SOD between the two groups (t value was -0.405, P > 0.05). The liver histological damages were observed in diabetes group, light microscope observation showed hepatocytes swelling, ballooned changing and fatty droplets clustering. CONCLUSION: The oxidant damage might exist in the liver diabetic model in mice.

Key concepts: Streptozotocin, Glutathione peroxidase, Superoxide dismutase, Internal medicine, Glutathione, Endocrinology, Diabetes mellitus, Nitric oxide

Related papers

Back to paper searchBrowse research topicsOriginal source
[A diabetic model for liver oxidant damage in mice]. — Research Paper | ScholarLens