Abstract
The liver is a primary site for xenobiotics detoxification, and its metabolism is readily altered by toxicity. The kidney is a common target for toxic xenobiotics due to its capacity to extract and concentrate toxic substances by highly specialized cells. So, they are the target organs of sodium fluoride toxicity. The aim of this review is to highlight on hepatorenal oxidative stress and pathophysiological changes induced by treatment of experimental animals with sodium fluoride. Our review shows fluoride toxicosis caused an elevation in the serum activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, acid phosphatase, and the level of total bilirubin, and reduction in the serum levels of total protein, albumin, and globulins, and serious histopathological changes in the hepaic tissues. Also, NaF administration caused increases in serum urea, creatinine, uric acid, sodium ions, and chloride ions levels and serious histopathological changes in the kidney tissues. Treatment of experimental animals with NaF induced oxidative stress in hepatic and renal tissues. It can be concluded that administration of sodium fluoride to experimental animals induced oxidative stress, serious hepatorenal histopathological changes, and disturbance in liver and kidney functions. So, human should be advised to decrease exposure to sodium fluoride to decrease the harmful effects of NaF on liver and kidney.
Highlights
The liver is the principal organ responsible for metabolism and involved in the metabolism of toxic compounds produced during systemic processes and exogenous toxins entering into the organisms from the environment [1] [2]
The liver is a primary site for xenobiotics detoxification, and its metabolism is readily altered by toxicity
The aim of this review is to highlight on hepatorenal oxidative stress and pathophysiological changes induced by treatment of experimental animals with sodium fluoride
Summary
The liver is the principal organ responsible for metabolism and involved in the metabolism of toxic compounds produced during systemic processes and exogenous toxins entering into the organisms from the environment [1] [2]. Excessive intake of fluoride for a prolonged period can produce injurious effects on the blood, teeth, skeleton and soft tissues such as the brain, thyroid, parathyroid glands, liver, and kidneys [24] [25]. Fluoride is first absorbed in the stomach, followed by its distribution through soft and hard tissues and urine excretion. These events occur in a pH-dependent manner because the coefficient of permeability of lipid bilayer membranes to hydrogen fluoride is much higher than that of ionic fluoride. Plasma fluoride concentration is a result of the relation between the levels of ingestion, and metabolism accounted by its deposition in calcified tissues and excretion. The aim of this review is to highlight on hepatorenal oxidative stress and pathophysiological changes induced by treatment effects of experimental animals with sodium fluoride
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