CAPÍTULO II: MARCO TEÓRICO
2.2 FUNDAMENTACIÓN TEÓRICA
2.2.10 Herramientas para la gestión financiera de empresas
This variant is one of the three polymorphic
variants, besides Albumins Mexico and Makiritare, to be
of Amerindian origin.
The dispersion of this variant is from the
Canadian and North American Indians [Naskapi, Montagnais,
Sioux, Athabascan (Navajo, Apache) and Shoshonean (Hopi)]
to Eskimos from Alaska and Labrador. Indians from the
middle and south USA, South Americans nor Africans,
Asians, Oceonics and Caucasians have yet to be found with
this variant. The discovery of this variant in so many
tribes have proven anthropological links, for example,
between the English-speaking, Anglican Naskapis and the
French-speaking, Roman Catholic Montagnais, both of whom
are Algonkian-speaking tribes. One plausible explanation
for its polymorphism is inbreeding through several generations
The genetic distribution of Albumin Naskapi on
Table 1.3 shows the heterozygotic frequency to be 8.48% and
the homozygous frequency as 0.36%.
This variant segretates genetically with Gc-1 140
phenotypes and the site of mutation is located between 8
8 9
residues 330 and 446 . This is on the B-turns of albumin
(Fig. 1.4) of Domain II, in between the high affinity binding
sites of bilirubin (Section 1.5.2.3 ) and on one of 164 secondary binding sites for medium chain fatty acids
It is not known if bindingsof these ligands are impaired.
An identical allomorph is albumin Mersin found
in high frequency amonst the Eti Turks of south eastern
TABLE 1.3 The genetic distribution of albumin Naskapi
Tribe Number AlNa/Na AiA/Na AlA/A
Naskapi (Canada) 203 1 54 148
Montagnais (Canada) 128 2 19 207
Sioux (N. America) 160 0 2 158
Athabashan (USA & Canada) 230 1 11 218
Eskimos (Labrador) 124 0 3 121
Eskimos (Canada & USA) 262 0 4 258
Total 1,107 4 93 1,010
% of Total 100 0.36 8.48 91.23
Adapted from Blumberg .
and 9.7% in Tarsus. This discovery of its similarities to
albumin Naskapi is anthropologically interesting because
it strongly suggests the ancestry of these Indians to be 89 from Mongoloid populations in Central and/or Eastern Asia
181 Albumin Naskapi binds more bromophenol blue
34
and thyroxine more tighly than albumin A. Both albumins
55
bind linolenic acid, linoleic acid and haemoglobin
181
equally well . Only albumin A binds riboflavin and
warfarin55. Reaction of penicillin with heterozygous
Albumin Naskapi produces four bands15.
1.6.2.9.4 Albumin Maku
This widely distributed variant is found in
tribes living in the Southern borders of Venezuela and
Brazil5111. The original sighting was in a captured Maku
woman and her three near relatives living among the
in two other individuals in adjacent north central Brazil
(Makiritare-2) and in the trihybrid population of Northern
Brazil (Belem III)303.
The migration of this variant is faster than
Albumin Naskapi at shorter (5-6 hr.) length of electrophoresis,
but this is reversed at longer (19 hr+) running times30
probably because Albumin Naskapi is able to bind more
charged ions during the longer running time to increase
its relative mobility.
1.6.2.9.5 Albumin Syracuse
This was found in a family of Swiss German descent.
Minimal separation was obtained on electrophoresis at
pH 8.6 but the variant separated well on cellulose acetate
. „ c .242
at pH 5.4
1.6.2.10 Dimeric Albumins
1.6.2.10.1 Warao
This dimer was found on two natives of British
Guyana11 and in five familial members of a Warao tribe living 12
in the Orinoco delta . This tribe is thought to originate
from the Andes and blood group-typing detected Karib or
Arawak Indian phenotypes.
This dimer constitutes 30% of the total albumin
content and can be separated easily into monomers by
heating at 56°C for 30 min. Susceptibility to dimerisation
may characterise this variant.
Its electrophoretic mobility is close to a^-
globulin on cellulose acetate and close to the fast-moving
a2~globulin in starch gel. It can be distinguished from
European dimers in the pH 6.0, but not in the 5.0 and
61
1.6.2.10.2 Albumin Makiritare
This dimer is found amongst the Makiritare and
the Piaroa tribes of Venezuela, and rhe Trio and Wajana
of Surinam. The average gene frequency is 0.014, arising
from a total of 41 affected individuals, out of 1,461 members on o of the four tribes: Makiritare, Warao, Trio and Wajana .
This hereditary dominant variant is also thought to be
alike Albumin Warao found in the Warao of Venezuela and 297
Wapishana of Guyana
1.6.2.10.3 Albumin Yanomama
This variant originates from the Yanomamo
Indians living in South Venezuela and Northern Brazil. They
separate on electrophoresis at pH 5.0 and 6.9 showing a 298
slight separation of monomers from dimers
1.6.2.10.4 Albumin dimers in Sweden, USA and Wales
Five carriers were found amongst some orthopaedic
patients in a Swedish clinic although a connection between
this hereditary anomoly with orthopaedics is unproven.
A large number of affected individuals were found in nine
of the 24 relatives of a proband, including a brother who
was homozygous.
The albumin dimer found in a healthy American
Negro carrier and 6 members of his family of nine1^7
could be dissociated into monomers after reduction and
.v . .. 136 alkylation
The electrophoretic mobility of the Welsh
dimer, which was the first reported case of hereditary 91
dimers is similar to a dimer found in the USA, except
that they differed in binding of alkaline haematin and
b
2
11 spanning three generations.
1.6.3 Non-hereditary transient bisalbuminemia
1.6.3.1 Introduction
Transient bisalbuminemia is a rarer phenomenon than
hereditary bisalbuminemia with about 50 reported cases from
1948 to 1979. It can be easily recognised as it appears in
lesser quantities than normal albumin during acute illness
as a fast (anodic) band adjacent to the normal allotype.
It usually disappears before complete recovery from illness
is secured. The fast band can be induced by ligand binding
or by pancreatic diseases.
Unlike hereditary bisalbuminemia, the drug- and
enzyme-induced forms are not usually clear distinct bands
. . . . 215
m vivo or in vitro, except within certain limits . Both albumins are usually immunochemically similar and
investigation of familial albumin excludes the hereditary
factor.
The initial reports of transient persistant
double albumins were by Glatthaar11*5 , Sandor22^,
42 > 274
Brodenstein and Rau and is reviewed by Tarnoky and
Porta215.
1.6.3.2 By Pancreatic Diseases
A fast albumin component was observed in a
47 year old woman with subacute pancreatitis with
hyperamylasemia. The concentration of the fast component
was later recognised to be directly proportional to the
serum amylase level. It constituted less than 50% of
the total serum albumin, even when the serum amylase 245
63
However, with the report of a aase of bisalbu-
minemia associated with chronic pancreatitis which was
indifferent to the level of amylase was reported, Lamotte- 155
Barillon suggested structural modification of albumin A
by trypsin.
Pancreatic enzymes were later shown to cause
formation of a more anodic component by limited proteolysis
of albumin A in a clinical case of pancreatitis with
hyperamylasemia. The same effect could be reproduced
in vitro by the limited action of chymotrypsin with carboxypeptidase A and B and elastasis-carboxypeptidase
A and B on albumin A. Trypsin acts merely to activate
6 8