Ph maintaun essential during citric acid formation
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Drug Metabolism and Pharmacokinetics
Citric acid is a normal metabolite and an intermediate in cellular oxidative metabolism. It is formed in the mitochondrion after condensation of acetate with oxaloacetate. The six-carbon acid is then successively degraded to a series of four-carbon acids, effectively accomplishing the oxidation of acetate in the cell [5]. Thus, citric acid is metabolized to carbon dioxide and water, and has only a transient effect on systemic acid-base status; it works as a temporary buffer component. Oxidation is virtually complete, and less than 5% of citrates are excreted in urine unchanged [79].
Citric acid is commonly consumed as part of a normal diet. Man’s total daily consumption of citric acid from natural sources and from food additive sources may exceed 500 mg/kg of body weight [4,5]. Citric acid is well absorbed from the gastrointestinal tract, and reacts with the enzyme citratase to yield oxaloacetic acid and acetic acid [27,70]. The total circulating citric acid in the serum of a man is approximately 1 mg/kg of body weight. Normal daily excretion in the urine of humans is 0.2-1.0 g [61].
Orally ingested citric acid is absorbed, and is generally regarded as a nontoxic material when used as an excipient. However, excessive or frequent consumption of citric acid has been associated with erosion of the teeth [1,4,5,71,72].
Citric acid (5 percent in the diet) did not depress food intake, but caused a loss in body weight gain and survival time in mice, with a slightly greater influence on mature animals. The effects on body weight gain and survival time may have resulted from the chelating ability of citric acid, which could impair absorption of calcium and iron. The use of large volumes of blood anti-coagulated with citrates has been shown to decrease plasma levels of calcium and magnesium [5,20].
Citric acid and citrates also enhance intestinal aluminum absorption in renal patients that may lead to increased and harmful serum aluminum levels. Although aluminum is an abundant terrestrial element, it is toxic to tissues, including the brain. It has therefore been suggested that patients with renal failure taking aluminum compounds to control phosphate absorption should not be prescribed citric acid and or citrate-containing products [1,4,73].
A study by Lacour et al indicates that citric acid supplementation together with a Ca-rich diet allows an increased retention of calcium and phosphorous in bone [74]. Addition of citric acidsupplements to a maize-soya diet enhanced the dialysability of calcium, magnesium, manganese and zinc. A a dose-dependent increase of lead and cadmium dialysability due to citric acidsupplementation was evident [75].
The result of a kinetic assessment of salivary secretory response to citric acidis citric acid provoked a rapid and short-lived salivary response that differs markedly from the one produced by other secretagogues, such as pilocarpine [76].
Citric acid is a normal metabolite and an intermediate in cellular oxidative metabolism. It is formed in the mitochondrion after condensation of acetate with oxaloacetate. The six-carbon acid is then successively degraded to a series of four-carbon acids, effectively accomplishing the oxidation of acetate in the cell [5]. Thus, citric acid is metabolized to carbon dioxide and water, and has only a transient effect on systemic acid-base status; it works as a temporary buffer component. Oxidation is virtually complete, and less than 5% of citrates are excreted in urine unchanged [79].
Citric acid is commonly consumed as part of a normal diet. Man’s total daily consumption of citric acid from natural sources and from food additive sources may exceed 500 mg/kg of body weight [4,5]. Citric acid is well absorbed from the gastrointestinal tract, and reacts with the enzyme citratase to yield oxaloacetic acid and acetic acid [27,70]. The total circulating citric acid in the serum of a man is approximately 1 mg/kg of body weight. Normal daily excretion in the urine of humans is 0.2-1.0 g [61].
Orally ingested citric acid is absorbed, and is generally regarded as a nontoxic material when used as an excipient. However, excessive or frequent consumption of citric acid has been associated with erosion of the teeth [1,4,5,71,72].
Citric acid (5 percent in the diet) did not depress food intake, but caused a loss in body weight gain and survival time in mice, with a slightly greater influence on mature animals. The effects on body weight gain and survival time may have resulted from the chelating ability of citric acid, which could impair absorption of calcium and iron. The use of large volumes of blood anti-coagulated with citrates has been shown to decrease plasma levels of calcium and magnesium [5,20].
Citric acid and citrates also enhance intestinal aluminum absorption in renal patients that may lead to increased and harmful serum aluminum levels. Although aluminum is an abundant terrestrial element, it is toxic to tissues, including the brain. It has therefore been suggested that patients with renal failure taking aluminum compounds to control phosphate absorption should not be prescribed citric acid and or citrate-containing products [1,4,73].
A study by Lacour et al indicates that citric acid supplementation together with a Ca-rich diet allows an increased retention of calcium and phosphorous in bone [74]. Addition of citric acidsupplements to a maize-soya diet enhanced the dialysability of calcium, magnesium, manganese and zinc. A a dose-dependent increase of lead and cadmium dialysability due to citric acidsupplementation was evident [75].
The result of a kinetic assessment of salivary secretory response to citric acidis citric acid provoked a rapid and short-lived salivary response that differs markedly from the one produced by other secretagogues, such as pilocarpine [76].
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