There are several vitamin B6 antagonists, which either compete for reactive sites of apoenzymes or react with PLP to form inactive compounds. The presence of a vitamin B6 antagonist in linseed meal is of particular interest to animal nutritionists. This substance was identified in 1967 as hydrazic acid and was found to have antibiotic properties (Parsons and Klostermann, 1967). Pesticides (e.g., carbaryl, propoxur or thiram) can be antagonistic to vitamin B6. Feeding a diet enriched with vitamin B6 prevented disturbances in the active transport of methionine in rats intoxicated with pesticides (Witkowska et al., 1992).
Digestion of vitamin B6 would first involve splitting the vitamin, as it is bound to the protein portion of foods. Vitamin B6 is absorbed mainly in the jejunum but also in the ileum by passive diffusion. Absorption from the colon is insignificant, even though colon microflora synthesize the vitamin. However, Durst et al. (1989) administered vitamin B6 in the cecum of sows and concluded that the vitamin was absorbed at this location. Little information is available on digestion and absorption of vitamin B6 in ruminants; however, large quantities of the vitamin are synthesized in the rumen.
Vitamin B6 compounds are all absorbed from the diet in the dephosphorylated forms. The small intestine is rich in alkaline phosphatases for the dephosphorylation reaction. Sakurai et al. (1992) reported that a physiological dose of pyridoxamine was rapidly transformed to pyridoxal in the intestinal tissues and then released in the form of pyridoxal into the portal blood. After absorption, B6 compounds rapidly appear in liver, where they are mostly converted into PLP, considered to be the most active vitamin form in metabolism. Pyridoxal phosphate is the major B6 form in goat milk, accounting for 75% of the vitamin B6 activity (Coburn et al., 1992). Both niacin (as nicotinamide adenine dinucleotide phosphate [NADP]-dependent enzyme) and riboflavin (as the flavoprotein pyridoxamine phosphate oxidase) are important for conversion of vitamin B6 forms and phosphorylation reactions (Kodentsova et al., 1993).
Although other tissues also contribute to vitamin B6 metabolism, liver is thought to be responsible for forming PLP found in plasma. Pyridoxal and PLP found in circulation are associated primarily with plasma albumin and red blood cell hemoglobin (Mehansho and Henderson, 1980). Pyridoxal phosphate accounts for 60% of plasma vitamin B6. Researchers do not agree on whether pyridoxal or PLP is the transport form of B6 (Driskell, 1984).
Only small quantities of vitamin B6 are stored in the body. The vitamin is widely distributed in various tissues, mainly as PLP or pyridoxamine phosphate. Vitamin B6 readily passes the placenta. Pyridoxal crosses the human placenta readily in both directions (Delport et al., 1991; Schenker et al., 1992). Pyridoxic acid is the major excretory metabolite of the vitamin, eliminated via the urine. Also, small quantities of pyridoxol, pyridoxal and pyridoxamine, as well as their phosphorylated derivatives, are excreted into the urine (Henderson, 1984). Vitamin B6 metabolism is altered in renal failure, as observed in rats exhibiting plasma pyridoxal phosphate 43% lower than controls (Wei and Young, 1994).
