Head trauma may lead to primary and secondary damages in neural tissue. Secondary factors that have been shown to develop subsequent to traumatic brain injury are ischemia, cerebral edema, and free oxygen radical-based lipid peroxidation [2–7]. Lipid peroxidation leads to dysfunction of membrane because of changes in the lipid structure of the membrane. Secondary cell injury is observed subsequent to inflammation, edema, chemotaxis, and increased vascular permeability with the development of free oxygen radicals, influencing other components of the cell [21–23].
Antioxidants inhibit lipid peroxidation by preventing the peroxidative chain reaction and/or picking up the reactive-oxygen derivatives. Endogenous antioxidants include mitochondrial cytochrome oxidase, SOD, catalase, glutathione peroxidase, glutathione-S-transferase, hydroperoxidase, and CoQ. CoQ10 is the only fat-soluble antioxidant synthesized endogenously, and it is present in tissues in the active form (reduced) independently from the diet .
The method described by Marmarou et al.  and modified by Uçar et al.  was used as the trauma model in our study. We designed the model to analyze the protective effect of CoQ10 on neuronal damage. In the method of Marmarou et al. , the area between the coronal and lambdoid sutures was targeted; a diffuse brain injury was caused by allowing an object of 450 g to fall freely from an altitude of two meters through a plexiglass tube. A possible fracture of the calvarium was prevented by a stainless steel plate stuck over the calvarium, similar to the method of our application. In the study of Marmarou et al., of the 54 rats, mortality and cranium fracture were found in 44% and 12.5%, respectively. We applied the moderate head-trauma model described by Uçar et al.  because Marmarou et al.'s model has both high mortality and risk of posttraumatic seizure. Accordingly, we arranged for an object of 450 g to fall through a plexiglass tube from an altitude of 70 cm onto target points around the coronal suture. The total scheduled number of rats in the trauma groups was 21 in our study. Among these, four rats died of trauma, and therefore, four additional rats were exposed to trauma and included into the study. Hence, a total of 25 rats were subjected to trauma and four (16%) died, while no cranium fracture was detected in any rat.
CoQ10, whose use in many neurological, cardiac, oncological, and immunological diseases has been studied, has been shown to be protective against different forms of tissue damage [25–28]. However, the efficacy of CoQ10 in a moderate head-trauma model has not been analyzed before.
Administration of a 10 mg/kg dose immediately after the trauma, which we applied, has been reported to have a protective effect against ischemic injury in experimental models, such as cerebral ischemia, tissue ischemia-reperfusion damage, and spinal cord trauma [12, 26, 29–32]. Li et al. , in a different study, showed that the administration of CoQ10 three hours after focal and global ischemia, which they formed by vessel occlusion in rats, does not have a protective effect against neural injury .
Ostrowski  induced cerebral ischemia by administrating intraventricular endothelin to rats in his study. He showed that SOD activity increased significantly in samples obtained by killing the subjects after he injected 10 mg/kg CoQ10 intraperitoneally at the end of the 24th hour. His interpretation of this result was that CoQ10 would decrease cerebral ischemic injury if the endogenous SOD activity was higher .
Erol et al.  found in their ischemia-reperfusion model that MDA levels were significantly lower in the group in which they applied a single dose of 10 mg/kg CoQ10 intraperitoneally than that in control group. They concluded that this could be attributable to CoQ10, which had an antioxidant effect by lowering lipid peroxidation.
Kerimoğlu et al.  analyzed the efficacy of CoQ10 on experimental spinal cord injury induced by placing extradural aneurysm clips at the T4-5 level in rats, and they found that the SOD activity of only the trauma-applied group was significantly lower than that of the control group (p < 0.05). Although the MDA levels were less than those in the control group, the result was not considered statistically significant. Again, although edema was significantly more frequent in the control groups compared to others during histopathological assessment, no statistical difference was observed in their study between the methylprednisolone, CoQ10, and methylprednisolone + CoQ10 groups in terms of edema and hemorrhage.
Herein, we measured (1) the levels of MDA, one of the products of lipid peroxidation, for evaluating oxidative stress, and (2) the activities of SOD and PON, for analyzing the antioxidant capacity. A statistically significant reduction (p < 0.05) in the MDA levels was seen in the group administered CoQ10 immediately after trauma (G4) compared to the group to which only trauma was applied (G2), and even lower results than that in the sham group (G1) were detected. When evaluating the results of SOD, an endogenous antioxidant enzyme functioning as a member of the defense mechanism against oxidative stress, values in the G4 group were found to be similar to that of G1, although that did not reach any statistical significance. These findings suggest that CoQ10 is a neuronal protector against oxidative damage in traumatic brain injury and that it functions by inhibiting lipid peroxidation. When assessing the data of PON, an antioxidant enzyme associated with the high-density lipoprotein structure, no difference was detected among the different groups.
From the results of our histomorphological assessment, it has been concluded that in rats, administration of CoQ10 after traumatic brain injury (G4 group) reduces vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic, and axonal edema in a statistically significant manner when compared to the G2 and G3 groups (p < 0.05). Moreover, by administering CoQ10, neuronal degenerative findings were significantly less intense (p < 0.05).