Building on the obtained resul…

Building on the obtained results, MDA content can be promoted via DZN treatment in the liver of rats.

The increased MDA content in the liver following DZN exposure was likely attributed to the inordinate generation of ROS, which could be explained in terms of hepatocyte enzyme leakage. It is argued that mitochondria are the primary source of ROS production [46,47]. Bergamini et al. [48] concluded that elevation of ROS tends to result in oxidative injuries of significant cellular macromolecules including lipids, proteins, and nucleic acids. The present investigation revealed that oxidative stress is induced by DZN treatment, since compromised antioxidant defenses and increased LPO in the liver provide relevant evidence for this finding. Our results are in accordance with the studies of El-Shenawy et al. [49] who demonstrated a significant increase in LPO level and a significant decrease in SOD, CAT and GPx activities in liver of rats exposed to DZN.

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One of the indispensable components of cellular antioxidant defenses are GSH redox cycles which play an essential role for the tissues to protect themselves against the ROS damage.

Serving as a non-enzymatic oxygen radical scavenger and as a substrate for differing enzymes like GPX, they take part in the removal of ROS [50]. GPX is claimed to be an essential selenocysteine-carrying enzyme for cellular antioxidant defense [51]. In this study, we observed a significant decrease in animals’ GPX activity treated by DZN. This can be explained owing to increased free radical production, as documented by enhanced MDA levels. The decrease of GPx activity induced by DZN may be attributable to a direct inhibitory oxidative effect on the enzyme. Biological macromolecules can be prevented from oxidative damage through antioxidant enzymes like SOD and CAT which are regarded as a primary defense.

SODs rapidly dismutate superoxide anion (O2 -•) to a less reactive molecule (H2O2), which is further degraded by CAT and GPx to water and oxygen [52]. The obtained results demonstrated a significant decrease in SOD activity followed by DZN treatment. Needless to mention, xenobiotics have the capacity to induce mitochondria superoxide radical production [53] and the amount of (O2 -•) formed in a cell can reach hazardous levels if SOD is inhibited. Superoxide radical often tends to be a potent inhibitor of CAT [54]. Moreover, several processes are involved in the depletion of antioxidant enzyme activity which could be attributed to a direct impact on the enzyme. These processes can include DZN-induced ROS generation, depletion of the enzyme substrates and down-regulation of transcription and translation. DZN toxicity can also account f