Blood circulation; Most of the BI2 in blood is methyl cobalamin; the same is true for other fluids including milk. 5'-Dcoxyadenosylcoba!amin and aquaeobalamin account for much smaller percentages; minor amounts of other, inactive, corrins also may be present. Most of the physiological forms of B12 are complexed to transcobal-amin-U. One very common polymorphic variant of transcobalamin-11 (259Arg) is less effective in delivering B12 to tissues than the reference form 259Pro (Namour etat., 2001).
A much smaller percentage of BI2 in blood is associated with transcobalamin-l or -111. Tissues can take up the transcobalamin-l I BI2 complex from circulating blood via its specilic receptor (cubilin), which is ubiquitously expressed. The mechanism of cubilin-medtated endocytosis is the same as in enteroeytes. The transcobalamins 1 or III. in contrast, are cleared only in the liver after binding to the asialoglycoprotein receptor. It has been suggested that this constitutes a protective mechanism for the selective excretion of potentially toxic corrins. since the transcobalamins I or 111 preferentially bind non-physiological BI2 analogs.
Bluod brain barrier: Cerebral microvessels contain megalin. suggesting its role in mediating the transfer of the B12tran scobalam i n -11 complex into cerebrospinal tluid (Zlokovic et at., 1996).
Matemo-fetal transfer. The B l2/transcobalamin-l I complex is taken up by the syn-trophoblast via megalin; the complex is the predominant form of maternally derived B12 in cytosol (Perez-D'Gregorio and Miller. 1998). The mode of B12 exit into fetal circulation is less clear.
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Whenever a doctor informs the parents that their child is suffering with Autism, the first & foremost question that is thrown over him is - How did it happen? How did my child get this disease? Well, there is no definite answer to what are the exact causes of Autism.