No abstract

Co-enzyme Q10 (Co-Q10) plays a key role in the cellular respiration for the production of ATP. The toxicity of quinones to the kidney appears to depend on variety of factors, including genetic polymorphisms and the individual’s comorbidites. The aim of the present study was to assess histologically the nephrotoxic effects of 6 weeks daily oral intake of Co-Q10 in experimental animals. Twenty-five Wistar rats weighing between 220-270 g were randomly divided into two groups: experimental “treated” and control “untreated” groups (n=15, n=10, respectively). The animals of the experimental group received 300 mg/kg daily dose of gelatinous capsules of Co-Q10 by oral gavage for six weeks. At the end of the study, all animals were sacrificed under general anesthesia and samples of the kidneys were excised for microscopic histopathological assessment of renal tissue using stain. The experimental group showed a range of mild to severe dilatation of Bowman’s space, with a mean corpuscular diameter of 294±38 µm that was significantly higher (p <0.05) than that of the untreated control group 208±31 µm. Shrinkage to complete destruction of the glomeruli was observed in the experimental group only. The long-term use of high doses of Co-Q10 had revealed a selective nephrotoxicity towards podocytes. This might be a risk factor leading to renal proximal tubular necrosis in rats and the subsequent renal function deterioration.

Coenzyme Q10 (Co-Q10) or ubiquinone plays an important role in the cellular metabolism. The safety profile of ubiquinone as a dietary supplement has been assessed in few sub-chronic toxicity studies. The aim of this study was to evaluate the possible hepatotoxic effect of long-term oral administration of an intermediate oral dose of Co-Q10 in experimental animals. Fifteen Wistar rats were treated with 300mg/kg daily oral doses of Co-Q10 using forced oral feeding for six weeks. Additional 5 healthy rats represented the control group for comparison. All rats were euthanized at the end of the 6th week. Then H and E stained histological sections of rats’ livers revealed vacuolation of hepatocytes, an increase in the diffusion of macrophages and the formation of microgranuloma most probably indicating a drug-induced injury. In conclusion, this study adds evidence supporting the potential hepatotoxic actions resulting from repeated administration of intermediate oral dose of Co-Q10 especially on the long-term.

Also called coenzyme Q10 (CoQ10), Ubiquinone is a vitamin-like endogenously produced factor essential for Adenosine triphosphate (ATP) mitochondrial production. Several research studies have reported that the exogenous supplementation of CoQ10 can lead to excessive salivation, especially in patients complaining of dry mouth. The objective of this study was to investigate the effect of long-term daily use of CoQ10 on the salivary glands in experimental animals by comparing the diameters of the glandular acini and striated ducts of a CoQ10-treated group and a control group. Twenty-five white albino rats were randomly divided into two groups; the control group consisted of 10 rats, while the CoQ10-treated group comprised 15 rats. The latter received daily oral treatment of 300 mg/kg CoQ10 for six weeks. Samples of the parotid, submandibular and sublingual glands were then dissected and examined histologically for comparative measurement of the diameters of the glands’ acini and striated ducts. The CoQ10 treated group had mean diameters of the serous acini for the parotid (79.8±11.2 μm) and submandibular (81.07±13.5 μm) glands that were significantly higher (P<0.05) than their diameters in the control group (67.5±8.4 μm and 73.3±13.8 μm), respectively. However, the difference was not statistically significant when comparing the diameters of striated ducts of the CoQ10-treated group and the control group. Continuous and prolonged exposure to exogenous ubiquinone may cause hypertrophic dilation of the acini within the salivary glands, namely the parotid and submandibular glands, which might be the underlying mechanism for excessive salivation. This can be considered a reversible adaptive response.