Coenzyme Q10 Ameliorates potassium cyanide-induced toxicosis in a mouse model

Autor: Francis Gitonga, Kipchumba Biwott, Grace Wairimu Gitau, Okanya Patrick Wafula, Peris Amwayi, Alfred Orina Isaac, James Nyabuga Nyariki
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Zdroj: Scientific African, Vol 12, Iss , Pp e00815- (2021)
Druh dokumentu: article
ISSN: 2468-2276
DOI: 10.1016/j.sciaf.2021.e00815
Popis: Potassium cyanide (KCN) is one of the most lethal and feared poison; which devastates cellular respiration resulting in death due to hypoxia. Several antidotes exist, but most face major limitations of safety and efficacy. Moreover, there is a need for new strategies to minimize post-exposure pathological sequel, which includes harmful oxidant and inflammatory changes. Coenzyme Q10 (CoQ10) is a powerful antioxidant, which has shown efficacy against chemical-induced toxicity. In the present study, the potential protective effect of CoQ10 against KCN-induced toxicosis was evaluated. Female Swiss white mice (3–4 weeks old) were divided into three treatment groups. The first group was used as the control, the second group was supplemented with 200 mg/kg of CoQ10 for one month before administration with 8 mg/kg of KCN. For this group, co-administration of CoQ10 and KCN was continued to the end of the experiment. The third group was administered 8 mg/kg of KCN. The experiment was terminated after 42 days post-treatment to enable investigations into the effect of KCN and CoQ10 on various physiological, biochemical, and cellular processes. The results of this study showed that KCN severely impaired the health of mice, more so, the neurological integrity. KCN-driven depletion of cellular glutathione (GSH) was noted in the liver and brain. This constitutes a characteristic impairment of the antioxidant capacity due to the induction of severe oxidative stress. CoQ10 significantly reinforced the neurological integrity and restored cellular glutathione (reduced form) in both the liver and brain, a clear indication of reduced oxidative stress. Remarkably, KCN-induced anemia, leukocytosis, and suppression of platelets were reversed by CoQ10 supplementation. Moreover, histopathological analysis revealed that CoQ10 supplementation blocked KCN-driven liver, kidney, and brain inflammation, and characteristic hypoxia-induced lesions. These findings open possibilities for further scrutiny and development of adjunct therapy utilizing CoQ10 to treat KCN poisoning.
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