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The intracellular nature of Brucella leads to rise in oxidative stress due to bacterial invasion, particularly at the site of predilection spleen and lymph nodes. The present study aimed to evaluate the erythrocytic and tissue specific oxidative stress responses induced during oil adjuvant killed Brucella melitensis vaccination. The results of the study clearly implicated a significant increase in level of catalase, and superoxide dismutase (SOD) activity and lipid peroxidation (LPO), and total protein content in erythrocytes after vaccination. The activity of glutathione-S-transferase (GST) was unaltered during the period of experiment. The catalase activity and GSH content was significantly increased in lung and spleen tissues. The tissues GST levels increased significantly in all tissues, while tissue SOD level increased significantly only in lung tissues. Thus, it can be inferred that oil adjuvant based Brucella vaccine induces negligible signs of inflammatory pathophysiology and supports the development of significant level of protection against virulent Brucella challenge. [ABSTRACT FROM AUTHOR]

Brucella melitensis, mainly responsible for human brucellosis, is considered as biological warfare. Being intracellular in nature Brucella induces oxidative stress due to bacterial invasion in organs like spleen and lymph nodes. The present study was aimed to evaluate the specific oxidative stress responses in erythrocytes and tissues induced by intranasal inoculation of killed Brucella whole cell protein antigen coupled with sodium acrylate nanoparticle adjuvant. Glutathione mediated nonenzymic antioxidant defense system and catalase have been observed to play a critical role in intracellular antioxidant defenses in vaccinated animals and also in maintaining an excellent milieu to induce an active immune potential. The antioxidant defenses in erythrocytes, liver, kidneys, lungs and spleen of vaccinated mice also maintained excellent redox homeostasis required for quality and effective protection without inflammatory pathophysiology. [ABSTRACT FROM AUTHOR]