A mechanistic overview of spinal cord injury, oxidative DNA damage repair and neuroprotective therapies

Abstract

Despite substantial development in medical treatment strategies scientists are struggling to find a cure against spinal cord injury (SCI) which causes long term disability and paralysis. The prime rationale behind it is the enlargement of primary lesion due to an initial trauma to the spinal cord which spreads to the neighbouring spinal tissues It begins from the time of traumatic event happened and extends to hours and even days. It further causes series of biological and functional alterations such as inflammation, excitotoxicity and ischemia, and promotes secondary lesion to the cord which worsens the life of individuals affected by SCI. Oxidative DNA damage is a stern consequence of oxidative stress linked with secondary injury causes oxidative base alterations and strand breaks, which provokes cell death in neurons. It is implausible to stop primary damage however it is credible to halt the secondary lesion and improve the quality of the patient’s life to some extent. Therefore it is crucial to understand the hidden perspectives of cell and molecular biology affecting the pathophysiology of SCI. Thus the focus of the review is to connect the missing links and shed light on the oxidative DNA damages and the functional repair mechanisms, as a consequence of the injury in neurons. The review will also probe the significance of neuroprotective strategies in the present scenario.

HIGHLIGHTS

• Spinal cord injury, a pernicious condition, causes excitotoxicity and ischemia, ultimately leading to cell death.

• Oxidative DNA damage is a consequence of oxidative stress linked with secondary injury, provoking cell death in neurons.

• Base excision repair (BER) is one of the major repair pathways that plays a crucial role in repairing oxidative DNA damages.

• Neuroprotective therapies curbing SCI and boosting BER include the usage of pharmacological drugs and other approaches.

Disclosure statement

Authors declare no conflict of interests.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.