Oral administration of Coenzyme Q10 protects mice against oxidative stress and neuro-inflammation during experimental cerebral malaria

Nyariki, James Nyabuga; Ochola, Lucy; Jillani, Ngalla E.; Nyamweya, Nemwel O.; Amwayi, Peris; Yole, Dorcas S.; Azonvide, Laurent; Isaac, Alfred

doi:10.1016/j.parint.2019.04.010

Cited by 31 publications

(14 citation statements)

References 102 publications

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“…However, other studies have demonstrated that oral CoQ 10 supplementation increases brain CoQ 10 concentrations in mice (Kwong et al, 2002;Matthews et al, 1998). Further, outcomes of previous experiments have shown a direct link between oral CoQ 10 supplementation and oxidative damage protection, neuroprotection and immunomodulation (Nyariki et al, 2019;Rashid et al, 2014).…”

Section: Discussionmentioning

confidence: 97%

Coenzyme Q10 nullified khat-induced hepatotoxicity, nephrotoxicity and inflammation in a mouse model

Kennedy

Okanya

Nyariki

et al. 2020

Heliyon

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The consumption of khat (Catha Edulis, Forsk) is on the rise despite the much publicized associated deleterious health effects. How chemicals present in khat, affect various physiological and biochemical processes requires further scrutiny. A clear understanding of these processes will provide an avenue for countering khat-driven negative effects using appropriate pharmacological and/or nutritional interventions.Aim of the study: The current study investigated the effect of khat on vital physiological and biochemical processes such as oxidative stress, inflammation and immune responses and the role of Coenzyme-Q 10 (CoQ 10 ), a potent antioxidant and anti-inflammatory, in modulating any negative effects due to khat exposure. Methodology: Three (3) weeks old forty (40) Swiss albino mice were randomly assigned into four treatment groups (n ¼ 10). The first group was the control that was not administered with khat or CoQ 10 . The second group received 200 mg/kg body weight (b/w) of CoQ 10 , while the third group received 1500 mg/kg b/w of khat extract and finally the forth group was co-treated with 200 mg/kg b/w of CoQ 10 and 1500 mg/kg b/w of khat extract. The experiment was conducted for 90 days after which samples were collected for physiological and biochemical analyses.Results: The effects of khat and CoQ 10 on the weights of brain, liver, kidney and spleen was determined. Administration of khat decreased the levels of RBCs and its subtypes (MCV, MCH, RDW-SD and RDW-CV), a clear indicator of khat-induced normochromic microcytic anemia. White blood cells (lymphocytes, monocytes, neutrophils and eosinophil) which are vital in responding to infections were markedly elevated by khat. Moreover, these results provide evidence for khat-induced liver and kidney injury as shown by increased biomarkers; AST, ALT, GGT and creatinine respectively. Standard histopathological analysis confirmed this finding for khat-driven liver and kidney injury. Further studies showed evidence for khat-induced inflammation and oxidative stress as depicted by increased levels of the pro-inflammatory cytokine TNF-alpha and elevation of GSH in the brain, liver and spleen. Remarkably, this is the first study to demonstrate the potential of CoQ 10 in ameliorating khat-induced negative effects as outlined. CoQ 10 supplementation restored the khat-induced reduction in RBC subtypes, and was protective against liver and kidney injury as shown by the appropriate biomarkers and standard histopathology analysis. The other significant finding was the CoQ 10 -driven normalization of GSH and TNF-α levels, indicating a protective effect from khat-driven oxidative stress and inflammation respectively. Conclusion: From this study, we conclude that CoQ 10 may be useful in nullifying khat-driven deleterious events among chronic khat users.

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Section: Discussionmentioning

confidence: 97%

Coenzyme Q10 nullified khat-induced hepatotoxicity, nephrotoxicity and inflammation in a mouse model

Kennedy

Okanya

Nyariki

et al. 2020

Heliyon

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“…However, compared to other techniques in the literature, our experimental model evaluated oxidative stress, adhesion and biomarkers in a different way (34,35). We measured the diamond adhesion score and investigated that clinical adhesion formation get decrease by the effect of coenzyme-Q-10 and we also obtained promising results of GSH-Px and SOD regarding anti-oxidant and anti-inflammatory process for pathological adhesion formation, we saw that utilization of coenzyme-Q-10 could be beneficial for intraabdominal protection after surgical procedures.…”

Section: Discussionmentioning

confidence: 99%

A novel coenzyme-Q approach for the prevention of postsurgical adhesion

et al. 2020

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Objective: Postoperative intraperitoneal adhesions are an unsolved and important problem in abdominal surgery. In the present study, the probable preventive role of coenzyme-Q in the development of peritoneal adhesions was investigated. Material and Methods: Sixteen Wistar Hannover male rats weighing 300-350 g were randomly separated into two groups of 8 rats each. The cecum was abraded with a sterile gauze until sub-serosal hemorrhage developed. A patch of peritoneum located opposite to the cecal abrasion was completely dissected. No treatment was given to Group 1. Group 2 received 30 mg/kg coenzyme-Q, which was injected 2 mL intraperitoneally. All the rats were sacrificed on the postoperative 21 st day, and after adhesions were scored macroscopically, tissue specimens of the peritoneum and bowel were subjected to histopathological investigation. Tissue and blood specimens were also taken for biochemical analysis to investigate antioxidant efficiency. Results: Adhesion scores were significantly different between the control group and the coenzyme-Q group (p= 0.001). According to the tissue levels of GSH-Px, MDA, and SOD levels, there was no significant difference between the study groups (p= 0.074, p= 0.208, p= 0.526). According to the plasma GSH-Px and SOD levels, there was significant difference between the groups (p= 0.002, p= 0.001), but the difference was not significant at MDA levels (p= 0.793). The differences between the pathological scores of the control and coenzyme-Q (p= 0.028 for fibrosis; p= 0.025 for inflammation) groups were statistically significant. Conclusion: This study confirms that coenzyme-Q is the potential application in the prevention of early postoperative adhesions.

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“…CoQ10 was also tested in rat and mouse models (Table 2), for its ability to counteract inflammatory conditions as druginduced [89], or in puncture-induced sepsis [90], or experimental cerebral malaria [91].…”

Section: Mitochondrial Nutrients: Action Mechanisms and Antioxidant Pmentioning

confidence: 99%

Potential roles of mitochondrial cofactors in the adjuvant mitigation of proinflammatory acute infections, as in the case of sepsis and COVID-19 pneumonia

et al. 2020

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Background The mitochondrial cofactors α-lipoic acid (ALA), coenzyme Q10 (CoQ10) and carnitine (CARN) play distinct and complementary roles in mitochondrial functioning, along with strong antioxidant actions. Also termed mitochondrial nutrients (MNs), these cofactors have demonstrated specific protective actions in a number of chronic disorders, as assessed in a well-established body of literature. Methods Using PubMed, the authors searched for articles containing information on the utilization of MNs in inflammatory disorders as assessed from in vitro and animal studies, and in clinical trials, in terms of exerting anti-inflammatory actions. Results The retrieved literature provided evidence relating acute pathologic conditions, such as sepsis and pneumonia, with a number of redox endpoints of biological and clinical relevance. Among these findings, both ALA and CARN were effective in counteracting inflammation-associated redox biomarkers, while CoQ10 showed decreased levels in proinflammatory conditions. MN-associated antioxidant actions were applied in a number of acute disorders, mostly using one MN. The body of literature assessing the safety and the complementary roles of MNs taken together suggests an adjuvant role of MN combinations in counteracting oxidative stress in sepsis and other acute disorders, including COVID-19-associated pneumonia. Conclusions The present state of art in the use of individual MNs in acute disorders suggests planning adjuvant therapy trials utilizing MN combinations aimed at counteracting proinflammatory conditions, as in the case of pneumonia and the COVID-19 pandemic.

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Oral administration of Coenzyme Q10 protects mice against oxidative stress and neuro-inflammation during experimental cerebral malaria

Cited by 31 publications

References 102 publications

Coenzyme Q10 nullified khat-induced hepatotoxicity, nephrotoxicity and inflammation in a mouse model

Coenzyme Q10 nullified khat-induced hepatotoxicity, nephrotoxicity and inflammation in a mouse model

A novel coenzyme-Q approach for the prevention of postsurgical adhesion

Potential roles of mitochondrial cofactors in the adjuvant mitigation of proinflammatory acute infections, as in the case of sepsis and COVID-19 pneumonia

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