Sporotrichosis-induced oxidative imbalance in liver and kidneys of rats infected with Sporothrix brasiliensis: renoprotective effects of farnesol.

Sporothrix brasiliensis is the most virulent species of the genus Sporothrix. Oxidative stress is a key defense mechanism to eliminate this pathogen through generation of reactive oxygen species (ROS). However, S. brasiliensis has developed mechanisms to counteract this response, contributing to its persistence in the host. This paradoxically leads to excessive ROS production in host tissues, inducing oxidative stress. Bearing this in mind, the use of plant-based natural products such as farnesol (terpene) is considered an approach to attenuate oxidative stress, as this compound is known to possess radical scavenging properties. The aim of this study was to determine whether oral administration of farnesol (100 mg/kg) might prevent or attenuate S. brasiliensis-induced in rat renal and hepatic oxidative stress. Renal ROS, thiobarbituric acid reactive substance (TBARS) levels, and both hepatic and renal glutathione S-transferase (GST) activity were significantly higher in infected (group C) compared to uninfected animals (group A), while catalase (CAT) activity was significantly lower. No significant differences were observed between groups regarding hepatic ROS and TBARS levels, as well as superoxide dismutase activity. Farnesol administered to infected animals (group D) attenuated the rise in renal ROS and TBARS levels, as well as GST activity compared to group C. In conclusion, data demonstrated that S. brasiliensis infection induced renal oxidative stress mediated by elevation in ROS levels, initiating membrane lipid damage and diminished CAT activity. The protective effects of farnesol may be attributed to a synergistic effect of its ROS-scavenging ability, diminished lipid damage, and enhanced GST activity.