Effects of melatonin on oxidative stress in streptozotocin-induced diabetic rats

Alice C. Maritim, Brian H. Moore, Ruth A. Sanders, John B. Watkins

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Oxidative stress plays an important role in diabetes and other oxygen- related diseases. Melatonin, a pineal hormone thought to be a scavenger of oxygen radicals and a potentially advantageous therapeutic agent in diseases having oxidative stress, was administered (10 mg/kg ip, in gum tragacanth to prolong its absorption, once a day for 4 successive days) to normal and 30- day streptozotocin-induced diabetic Sprague-Dawley rats, after which markers of oxidative stress were assessed in the liver, kidney, intestine, and spleen. Alanine and aspartate aminotransferase activities in serum, which were increased after diabetes, were not increased further by melatonin administration, indicating that there was no melatonin-related liver toxicity. Most melatonin-induced effects were seen in the liver, and very few in extrahepatic tissues. In livers of diabetic rats, reduced concentration of nitrite and increased lipid peroxidation were both restored to normal levels following treatment with melatonin. Hepatic glutathione peroxidase activity was not changed in diabetics, but was decreased after melatonin administration in both normal and diabetic animals. Total glutathione concentrations were significantly decreased in livers of all diabetics and were not normalized by melatonin treatment. Hepatic superoxide dismutase activity was elevated following melatonin dosing in normal rats, but dropped below normal levels in diabetic rats and was not restored by melatonin treatment. Glutathione S-transferase activity was higher than normal in melatonin-dosed normal rat livers. These results suggest that after 4 days of administration, melatonin may enable various enzymes of the hepatic antioxidative defense system to better detoxify harmful oxygen radicals without producing overt toxicity in a disease such as diabetes.

Original languageEnglish
Pages (from-to)161-166
Number of pages6
JournalInternational Journal of Toxicology
Volume18
Issue number3
DOIs
StatePublished - May 1999

Fingerprint

Oxidative stress
Melatonin
Streptozocin
Rats
Oxidative Stress
Liver
Medical problems
Toxicity
Reactive Oxygen Species
Tragacanth
Glutathione Peroxidase
Nitrites
Aspartate Aminotransferases
Glutathione Transferase
Alanine Transaminase
Lipid Peroxidation
Superoxide Dismutase
Intestines
Glutathione
Sprague Dawley Rats

Keywords

  • Antioxidant
  • Catalase
  • Diabetes
  • Free Radical
  • Glutathione
  • Glutathione Peroxidase
  • Glutathione Reductase
  • Glutathione S-Transferase
  • Lipid Peroxidation
  • Melatonin
  • Oxidative Stress
  • Rat
  • Streptozotocin
  • Superoxide Dismutase
  • Thiobarbituric Acid

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Effects of melatonin on oxidative stress in streptozotocin-induced diabetic rats. / Maritim, Alice C.; Moore, Brian H.; Sanders, Ruth A.; Watkins, John B.

In: International Journal of Toxicology, Vol. 18, No. 3, 05.1999, p. 161-166.

Research output: Contribution to journalArticle

Maritim, Alice C. ; Moore, Brian H. ; Sanders, Ruth A. ; Watkins, John B. / Effects of melatonin on oxidative stress in streptozotocin-induced diabetic rats. In: International Journal of Toxicology. 1999 ; Vol. 18, No. 3. pp. 161-166.
@article{59602d1f4b35424ca95f90996d030061,
title = "Effects of melatonin on oxidative stress in streptozotocin-induced diabetic rats",
abstract = "Oxidative stress plays an important role in diabetes and other oxygen- related diseases. Melatonin, a pineal hormone thought to be a scavenger of oxygen radicals and a potentially advantageous therapeutic agent in diseases having oxidative stress, was administered (10 mg/kg ip, in gum tragacanth to prolong its absorption, once a day for 4 successive days) to normal and 30- day streptozotocin-induced diabetic Sprague-Dawley rats, after which markers of oxidative stress were assessed in the liver, kidney, intestine, and spleen. Alanine and aspartate aminotransferase activities in serum, which were increased after diabetes, were not increased further by melatonin administration, indicating that there was no melatonin-related liver toxicity. Most melatonin-induced effects were seen in the liver, and very few in extrahepatic tissues. In livers of diabetic rats, reduced concentration of nitrite and increased lipid peroxidation were both restored to normal levels following treatment with melatonin. Hepatic glutathione peroxidase activity was not changed in diabetics, but was decreased after melatonin administration in both normal and diabetic animals. Total glutathione concentrations were significantly decreased in livers of all diabetics and were not normalized by melatonin treatment. Hepatic superoxide dismutase activity was elevated following melatonin dosing in normal rats, but dropped below normal levels in diabetic rats and was not restored by melatonin treatment. Glutathione S-transferase activity was higher than normal in melatonin-dosed normal rat livers. These results suggest that after 4 days of administration, melatonin may enable various enzymes of the hepatic antioxidative defense system to better detoxify harmful oxygen radicals without producing overt toxicity in a disease such as diabetes.",
keywords = "Antioxidant, Catalase, Diabetes, Free Radical, Glutathione, Glutathione Peroxidase, Glutathione Reductase, Glutathione S-Transferase, Lipid Peroxidation, Melatonin, Oxidative Stress, Rat, Streptozotocin, Superoxide Dismutase, Thiobarbituric Acid",
author = "Maritim, {Alice C.} and Moore, {Brian H.} and Sanders, {Ruth A.} and Watkins, {John B.}",
year = "1999",
month = "5",
doi = "10.1080/109158199225440",
language = "English",
volume = "18",
pages = "161--166",
journal = "International Journal of Toxicology",
issn = "1091-5818",
publisher = "SAGE Publications Inc.",
number = "3",

}

TY - JOUR

T1 - Effects of melatonin on oxidative stress in streptozotocin-induced diabetic rats

AU - Maritim, Alice C.

AU - Moore, Brian H.

AU - Sanders, Ruth A.

AU - Watkins, John B.

PY - 1999/5

Y1 - 1999/5

N2 - Oxidative stress plays an important role in diabetes and other oxygen- related diseases. Melatonin, a pineal hormone thought to be a scavenger of oxygen radicals and a potentially advantageous therapeutic agent in diseases having oxidative stress, was administered (10 mg/kg ip, in gum tragacanth to prolong its absorption, once a day for 4 successive days) to normal and 30- day streptozotocin-induced diabetic Sprague-Dawley rats, after which markers of oxidative stress were assessed in the liver, kidney, intestine, and spleen. Alanine and aspartate aminotransferase activities in serum, which were increased after diabetes, were not increased further by melatonin administration, indicating that there was no melatonin-related liver toxicity. Most melatonin-induced effects were seen in the liver, and very few in extrahepatic tissues. In livers of diabetic rats, reduced concentration of nitrite and increased lipid peroxidation were both restored to normal levels following treatment with melatonin. Hepatic glutathione peroxidase activity was not changed in diabetics, but was decreased after melatonin administration in both normal and diabetic animals. Total glutathione concentrations were significantly decreased in livers of all diabetics and were not normalized by melatonin treatment. Hepatic superoxide dismutase activity was elevated following melatonin dosing in normal rats, but dropped below normal levels in diabetic rats and was not restored by melatonin treatment. Glutathione S-transferase activity was higher than normal in melatonin-dosed normal rat livers. These results suggest that after 4 days of administration, melatonin may enable various enzymes of the hepatic antioxidative defense system to better detoxify harmful oxygen radicals without producing overt toxicity in a disease such as diabetes.

AB - Oxidative stress plays an important role in diabetes and other oxygen- related diseases. Melatonin, a pineal hormone thought to be a scavenger of oxygen radicals and a potentially advantageous therapeutic agent in diseases having oxidative stress, was administered (10 mg/kg ip, in gum tragacanth to prolong its absorption, once a day for 4 successive days) to normal and 30- day streptozotocin-induced diabetic Sprague-Dawley rats, after which markers of oxidative stress were assessed in the liver, kidney, intestine, and spleen. Alanine and aspartate aminotransferase activities in serum, which were increased after diabetes, were not increased further by melatonin administration, indicating that there was no melatonin-related liver toxicity. Most melatonin-induced effects were seen in the liver, and very few in extrahepatic tissues. In livers of diabetic rats, reduced concentration of nitrite and increased lipid peroxidation were both restored to normal levels following treatment with melatonin. Hepatic glutathione peroxidase activity was not changed in diabetics, but was decreased after melatonin administration in both normal and diabetic animals. Total glutathione concentrations were significantly decreased in livers of all diabetics and were not normalized by melatonin treatment. Hepatic superoxide dismutase activity was elevated following melatonin dosing in normal rats, but dropped below normal levels in diabetic rats and was not restored by melatonin treatment. Glutathione S-transferase activity was higher than normal in melatonin-dosed normal rat livers. These results suggest that after 4 days of administration, melatonin may enable various enzymes of the hepatic antioxidative defense system to better detoxify harmful oxygen radicals without producing overt toxicity in a disease such as diabetes.

KW - Antioxidant

KW - Catalase

KW - Diabetes

KW - Free Radical

KW - Glutathione

KW - Glutathione Peroxidase

KW - Glutathione Reductase

KW - Glutathione S-Transferase

KW - Lipid Peroxidation

KW - Melatonin

KW - Oxidative Stress

KW - Rat

KW - Streptozotocin

KW - Superoxide Dismutase

KW - Thiobarbituric Acid

UR - http://www.scopus.com/inward/record.url?scp=0032891418&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032891418&partnerID=8YFLogxK

U2 - 10.1080/109158199225440

DO - 10.1080/109158199225440

M3 - Article

AN - SCOPUS:0032891418

VL - 18

SP - 161

EP - 166

JO - International Journal of Toxicology

JF - International Journal of Toxicology

SN - 1091-5818

IS - 3

ER -