Abstract
Sepia ink, a black suspension of melanin granules, is a multifunctional marine bioactive material. The present study aims to evaluate the ameliorative effect of the ink extract (IE) of the cuttlefish (Sepia officinalis) during high dosage administration of the FA in rats. Kidney injury induced by a single oral dose of FA (250 mg /kg). Eighteen male Wistar albino rats were the control, FA group, and FA+ IE group (250mg/kg). The IE showed a significant ameliorative effect against hepatorenal injury induced by high intake of FA as evident by decreasing the levels of serum aminotransferases (AST and ALT), urea, creatinine, uric acid, and significantly increased total serum albumin. Treatment with IE normalized the antioxidant status of the injured animals by reducing the MDA and the significant increase in the levels of GSH and CAT. The present study revealed that IE had an insightful effect against hepatorenal injury-induced following high intake of FA in rats, as it alleviates the alterations in the oxidative stress markers.
Highlights
Folate is a water-soluble vitamin that is required for cell growth and development [1]
The present study aims to evaluate the ameliorative effect of the ink extract (IE) of the cuttlefish (Sepia officinalis) during high dosage administration of the folic acid (FA) in rats
The present study revealed that IE had an insightful effect against hepatorenal injury-induced following high intake of FA in rats, as it alleviates the alterations in the oxidative stress markers
Summary
Folate is a water-soluble vitamin that is required for cell growth and development [1]. Hypervitaminosis has been linked to liver injury, according to recent research [3]. In Egypt, folic acid (FA) is a synthetic folate that is added to fortify Baladi bread [4]. Increased folic acid use has been linked to liver damage (2015). Concerns about the safety of long-term high-dose folic acid supplementation that results in the accumulation of unmetabolized folic acid (UFA) have been growing [6]. Field et al suggested that the development of liver injury as a result of UFA could be related to enzyme inhibition [7]. Unmetabolized homocysteine accumulates after a high dose of UFA, according to a significant body of research [6]. Evidence suggests that high levels of homocysteine are associated with negative consequences such as oxidative stress and non-alcoholic fatty liver disease (NAFLD) [8]
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