Research Article: Effects of oxidative stress on liver, brain and spinal cord of rats using L-NAME and treated with hydroxyurea. A model of sickle cell complication1

Date Published: May 8, 2020

Publisher: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia

Author(s): Abilio Torres dos Santos, Iandara Schettert Silva, Maria Lucia Ivo, Camila Tozaki Rodrigues, Eduardo Benedetti Parisotto, Rondon Tosta Ramalho, Geanlucas Mendes Monteiro.

http://doi.org/10.1590/s0102-865020200030000001

Abstract

To analyze the serum levels of nitric oxide and correlate them with the levels of thiobarbituric acid reactive substances (TBARS) in liver, brain and spinal cord of animals using L-NAME and treated with hydroxyurea.

Eighteen male albino Wistar rats were divided into three groups. NG-nitro-L-arginine methyl ester (L-NAME) was intraperitoneally administered to induce oxidative stress. TBARS and plasma nitric oxide levels were analyzed in all groups. Histopathology of the liver and vascular tissue was performed.

Statistically significant differences were seen in liver, brain and spinal cord TBARS levels.

Following the use of L-NAME, hepatic tissue increased the number of Kupffer cells as oxidative stress and inflammatory response increased. The use of L-NAME caused an increase in lipid peroxidation products and, consequently, in oxidative stress in animals. Hydroxyurea doses of 35 mg / kg / day reduced TBARS values in liver, brain and spinal cord.

Partial Text

Sickle cell disease (SCD) is a term associated with the group of hemoglobinopathies, characterized by the mutation of chromosome 11 that causes the change of a nitrogen base pair (adenine → thymine) in the sixth position of the beta globin chain; consequently, this change causes a replacement of glutamic acid with a valine, thus producing hemoglobin S (HbS)1.

All procedures and protocols were followed as approved by the Ethics and Animal Use Committee / CEUA / UFMS N. 646/2014.

By histopathological assays, after the use of L-NAME, liver tissue showed an increase in the number of Kupffer cells as oxidative stress and inflammatory response rose.

 

Source:

http://doi.org/10.1590/s0102-865020200030000001

 

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