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Anthropological survey on red cell glutathione peroxidase (GPX1) polymorphism in Central Western Africa A tentative hypothesis on the interaction between GPX1.13307902 and Hb.pdfS allelic products

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AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 79217-224 (1989)
Anthropological Survey on Red Cell Glutathione Peroxidase
(GPXI) Polymorphism in Central Western Africa: a Tentative
Hypothesis on the Interaction between GPXI*2 and Hbp*S
Allelic Products
GIOVANNI DESTRO-BISOL AND GABRIELLA SPEDINI
Departments of Human and Animal Biology and Anthropology, University
of Rome “La Sapienza,” 1-00185Rome (G.S.)and Institute of Forensic
Medicine, Catholic University, 1-00168,Rome (G.D.-B.),Italy
KEY WORDS
Mbugu, Sango, Goun, Bamileke
ABSTRACT
Phenotype and allele frequencies for erythrocyte glutathione
peroxidase (GPX1) polymorphism are reported in the Mbugu and Sango
(Central African Republic), Goun (Benin), and Bamileke (Cameroon) ethnic
groups. The GPX1*2 allele frequencies (from 0.012 in the Sango to 0.058 in the
Bamileke) fit into the range of the data already known for the Subsaharan
populations. The value of GPXl*2 for study of the genetic admixture between
Negro and Pygmy populations is suggested. Three different unusual GPXl
electrotypes are described. Finally, we hypothesize a n interaction between
GPX1*2 and Hb beta*S allelic products occurring in the sickle cells infected by
Plasmodium falciparum.
For almost 15 years the staff of the Laboratory of Anthropology at the University of
Rome “La Sapienza” has been actively engaged in the anthropogenetic study of the
Subsaharan populations. In particular, we
have concentrated on the biological interrelations of the Subsaharan populations and the
possible interactions between the strong selective forces to which these groups are exposed
and some of their biological characteristics
(Spedini et al., 1980a,b, 1981, 1982, 1983,
1985-86, 1986).
Erythrocyte glutathione peroxidase (GPX1:
EC 1.11.1.9) (Mills, 1957) is a selenoenzyme
(Flohe et al., 1973; Rotruck et al., 1973) that
catalyzes the oxidation of reduced glutathione (GSH) by peroxides, and is thus vital in
the defence against oxidative damage. The
importance of this enzyme within the biochemical pathway of red blood cells is shown
by the haemolytic anaemia caused by GPXl
deficiency (Necheles et al., 1970), along with
the noticeable variations of GPXl activity
observed in various haemolytic diseases: HbS
(Chiu and Lubin, 1979; Das and Nair, 1980;
Ponzetto-Zimmermann and Natta, 1981; Beretta et al., 1983); GGPD deficiency (Beutler,
1977; Swarup-Mitra, 1977; Gerli et al., 1982;
0 1989 ALAN R. LISS, INC.
Mavelli et al., 1984); alpha-thalassaemia
(Beutler et al., 1977); and beta-thalassemia
(Gerli et al., 1980).
The electrophoretic polymorphism of GPXl,
first reported in US blacks (Beutler and West,
1974), is determined by the two codominant
alleles GPX1*1 and GPX1*2 (following the
nomenclature introduced by Meera Khan et
al., 1984a).The previous GPXl studies (Beutler
and West, 1974; Beutler et al., 1974; Nurse
and Jenkins, 1976; Board, 1983; Meera Khan
et al., 1984a, 1986; Destro-Bisol et al., 1986;
Meera Khan, 1986) have pointed out that
GPX1*2 is present only among Subsaharans
and in populations with a probable African
genetic heritage, thus supporting the theory
of “African marker” value of GPX1*2 (Meera
Khan et al., 1986).
Some rare variants have been observed:
GPXl “Musi” (Beutler et al., 1974); GPXl
“Lebanese” homozygous and heterozygous
variants (Board, 1983); GPXl “Djuka” or
GPXl 3-1 and GPXl 4-1 (Meera Khan et al.,
1984b).However, there have been no reported
family studies demonstrating the genetic
Received March 20, 1987; accepted July 20, 1988.
218
G. DESTRO-BISOL AND G. SPEDINI
inheritance of any of these variants. Recently
Prof. P. Meera Khan informed us that he had
encountered three further GPXl variants,
including a silent allele in some Jewish
populations.
Interestingly, the catalytic activity of the
GPX1*2 allele product was found to be almost
twice that of GPX1*1 (Meera Khan et al.,
1986). Given the importance of the GPXl
physiological role and the considerably higher
activity of the GPX1*2 allele product, it
would be interesting to investigate a possible
selective role of the latter polymorphism.
We have previously reported the GPXl frequencies obtained from the Beti, Bateke, and
Babenga populations of the Congo (DestroBisol et al., 1986).In this paper we present the
GPXl data relative to the Goun (Benin),
Mbugu and Sango [Central African Republic
(CAR)], and Bamileke (Cameroon) populations. All the groups examined have been
settled in Central-Western Africa for some
time, where they and other populations have
interacted sometimes peacefully, sometimes
violently, and where there has been a great
spreading of malarial parasites (Fig. 1).
POPULATIONS
According to the linguistic classification of
Greenberg (1980), the Goun, Sango, and
Mbugu populations belong to the non-Bantu
or West African family of the Niger-Congo
Fig. 1. Geographic location of the populations examined in this survey on GPXl polymorphism in CentralWestern Africa: 1,Mbugu;2, Sango;3, Bamileke;4, Goun;5,
cluster, while the Bamileke of Cameroon fit
into the Bantu “lato-sensu” group of the
Benue Congo family. The Goun live in the
southern region of Benin and the Mbugu and
Sango in the Basse Kotto district on the
banks of the Ubangui river in the CAR.
Details of the history and distribution of
some other genetic markers in the examined
populations are reported in Spedini et al.,
1980a and Destro-Bisol et al., 1987 for the
Goun; Spedini et al., 1983 and Destro-Bisol et
al., 1987 for the Mbugu and Sango; and
Spedini et al., 1988, in preparation for the
Bamileke.
MATERIALS AND METHODS
The material included blood samples from
45 Mbugu and 47 Sango of the Basse Kotto
district (CAR) collected in 1979 and from 18
Goun residing in Port0 Novo (Benin) collected in 1980. The methods of blood collection, shipment, and storage are reported in
Spedini et al. (1983). In addition, during a n
expedition led by G.S. in 1985 in SouthWestern Cameroon, 452 blood samples were
collected from a s many Bamileke residing in
three different parts of the Department of
Moungo: 259 from Manengole village, 116
from Kongsamba Town (including 11related
individuals), and 77 from Ndoungue Village,
of which 54 were from pregnant women. The
blood samples, obtained by venipuncture,
South Bateke; 6 , Babenga Pygmies; 7, North Bateke; 8,
Beti.
219
GLUTATHIONE PEROXIDASE IN AFRICA
were collected in K3-EDTA tubes a s in our
previous GPXl survey (Destro-Bisol et al.,
1986). The samples were separated, salinewashed, and then stored separately a s serum
and washed packed red cells a t -20°C within
12 hours of collection in the laboratory of the
Centres des Grandes Endemies a t Kongsamba. The samples were then flown on ice to
Rome within 12days and transported directly
to the Laboratory of Anthropology at the
University of Rome “La Sapienza,” where
they were stored at -30°C before electrophoresis.
Preparation of samples and electrophoretic
procedures were performed in accordance
with Meera Khan et al. (1984a), except that
0.05 M dithiothreitol (DTT) was used as lysis
solution instead of 0.1 M 2-mercaptoethanol
(2-ME).Samples exhibiting unusual patterns
were treated by 0.05 or 0.1 M DTT, 1M or 2 M
2-ME, or 0.05 M GSH.
For gene counting only unrelated individuals were taken into account.
RESULTS
Of the 562 samples analyzed, 492 were easily typed a s one of the previously reported
GPXl 1,2-1, and 2 phenotypes; the remaining
70 samples showed unusual electrotypes (Fig.
2). I n order to avoid any mistyping caused by
protein denaturation, the samples exhibiting
unusual electrotypes were treated,with 2-ME
and GSH solutions (Beutler and West, 1974),
but no change in the electrophoretic pattern
was observed in any of these samples.
Of the Bamileke samples, 53 showed a single GPXl band slightly faster than that of
the GPXl 1 type. This unusual electrotype
was named “Bamileke.” It was possible to
perform a family analysis for one carrier of
“Bamileke” variant of the Nkongsamba
group, who was excluded from gene counting.
The paternity was confirmed by the determination of 12 other gene markers, including
red cell enzymes and serum proteins; both
parents of the propositus showed the GPXl 1
phenotype. This sample and the other identical variants were therefore considered a s
GPXl 1 types. In addition, GPXl 1 and
“Bamileke” electrotypes were found to be
undistinguishable by ultrathin-layer polyacrylamide gel isoelectric focusing in the range
of pH 4-6 (Destro-Bisoland Briziobello, 1987).
Thirteen Mbugu and four Sango showed
two different unusual electrotypes, which we
named “A” and “B.” For these last two variants, family data were not available; as a
precautionary measure, they were excluded
from gene counting. The results are summarized in Table 1.
+
0
I
PHENOTYPE
I
2-2 ’BAM
n
X 2-1
“B’
1-1
Fig. 2. Diagrammatic representation and zymograms
of some GPXl phenotypes. Variants “A” and “B’ were
2.2
‘BAM’
‘A’
2-1 ‘6’
drawn following the interpretation of Prof. Meera Khan
(see text).
220
G. DESTRO-BISOLAND G. SPEDINI
TABLE 1. Distribution of GPXI phenotypes and allele frequencies in the examined populations1
Pouulation
1
CAR
Mbugu2
0bserved
Expected
Sang03
Observed
Expected
Benin
Goun
Observed
Expected
Cameroon
Barnileke
(Manengole)
Observed
Expected
(Kongsambayl
Observed
Exuected
(Ndo~ngue)~
Observed
Expected
Total6
Observed
Expected
GPXl phenotype
2-1
2
Total
Allele frequency
GPX1*1
GPX1*2
X::
29
29.1
3
2.8
0
0.1
32
32.0
0.953 f 0.026
0.047
-
42
42.0
1
1.0
0
0.0
43
43.0
0.988 j, 0.010
0.012
-
17
17.0
1
1.0
0
0.0
18
18.0
0.972 zk 0.027
0.028
-
228
227.9
30
30.1
1
259
259.0
0.938 f 0.011
0.062
0.001
1.0
91
90.6
13
13.9
1
0.5
105
105.0
0.929 k 0.018
0.071
0.562
73
73.1
4
3.9
0
0.1
77
77.0
0.974 j, 0.01 3
0.026
-
392
391.3
47
48.2
2
1.5
441
441.0
0.942 f 0.008
0.058
0.188
lThese data were communicated at the Fifth Congress of the European Anthropological Association, Lisboa, September 28 to October 4,
1986.
2Ten “A”and three “B’ variants were excluded.
3Three “ A and one “B’ variants were excluded.
4Includes eight “Bamileke” variants; 11 related individuals (including one GPXl “Bamileke”, one GPXl 2, and nine GPX1) were excluded.
SIncludes 44 “Bamileke” variants.
6No statistically significant difference was found among the three Barnileke subgroups by a classical chi-square test for comparison.
DISCUSSION
Unusual variants
In terms of electrophoretic mobility and the
single banded pattern, the variant phenotypes encountered among the Bamileke resemble the GPXl “Musi” variant, previously
found in two related individuals affected by
refractory anaemia and in several cord blood
samples (Beutler et al., 1974). It is interesting
to note that 33 of the 53 “Bamileke” variants
were found in the group of 54 pregnant
women included in the Ndongue sample.
Unfortunately, the “Musi” sample was not
available for a comparison (Prof. E. Beutler,
Scripps Foundation, La Jolla, CA, personal
communication). However, the fact that for
both the “Bamileke” and the “Musi” variants
the patterns of inheritance did not confirm
the genetic origin of the changed electrophoretic mobility supports the identity of these
two variants.
It is worth mentioning that a remarkable
decrease in the selenium content was found
in both the blood of pregnant women and in
cord blood (Rudolph and Wong, 1978; Behne
and Wolters, 1979; Butler et al., 1982;Pleban
et al., 1982).These findings led us to suggest
tentatively that a scarcity of blood selenium
could be related to the changed electrophoretic mobility of the “Musi” variants found in
the cord blood samples and of the “Bamileke”
variants found among the pregnant women
of Ndoungue. It is well known that lack of a n
inorganic element of the prosthetic group of
proteins can cause a change in their conformation and, consequently, a different electrophoretic mobility. Obviously our hypothesis await further experimental confirmations.
Two different unusual electrophoretic variants, which we have called “A’ and “B,”
were found in the CAR populations. They
were apparently heterozygotes for the common GPXl allele and two further GPXl
alleles. “A” and “B” variants showed a n electrophoretic mobility very similar to those of
the “Lebanese variants” (Board, 1983).However, owing to the low activity of the “Lebanese variants” a t our disposal, we could not
reach a definite conclusion. Prof. P. Meera
221
GLUTATHIONE PEROXIDASE IN AFRICA
Khan, after examining the photograph shown
in Figure 2, suggested that the “ A ’ and “B”
variants could be respectively the GPXl 3-1
(found among the Djuka of Surinam: Meera
Khan et al., 1986) and GPXl 4-1 (previously
found in a Negro: Meera Khan et al., 1984b).
The Djuka of Surinam are descendants of
captives from Central-Western Africa and
probably from a wider region of West Africa
(Meera Khan et al., 1986). The geographic
location of their forefathers is therefore in
accordance with the suggested identity between the GPXl “Djuka” and “A” variants.
GPXl*2 allele as anthropological marker
All the populations examined were characterized by polymorphic frequencies of GPX1*2
(from 0.012 in the Sango to 0.058 in the Bamileke), which fit into the range of values
reported for the Subsaharan populations
(Table 2). The GPX1*2 allele was not found in
any population of non-African origin, with
the exception of Ashkenazy Jews of the
United States and Punjabis of India; this
finding could be the result of their ancient
genetic admixture with African populations
(Mourant et al., 1976; Meera Khan et al.,
1984a).The data obtained by us strongly support the theory of the “African marker” value
of GPX1*2 (Meera Khan et al., 1984a) and
enable us to outline more exhaustively the
GPXl distribution in Subsaharan Africa.
When we group the Sudanic population on
one side and the Bantu on the other, the
GPX1*2 frequencies do not show a noteworthy variation. These results are in accordance with previous findings on other genetic
polymorphisms in Subsaharan Africa.
As to the Pygmies, data obtained from the
Babenga of the Congo are in line with the low
frequencies (Babinga of the CAR, Twa of
Rwanda) or absence (Mbuti of Zaire and
Western Pygmies from Cameroon) of the
GPX1*2 noticed in the other Pygmy groups.
TABLE 2. GPXl x2 allele freouencies reDorted in Drevious studies
Population
Negroids
Bantus
Bamileke
Beti
North Bateke
South Bateke
Hutu
Tutsi
Denasena
Zulu
West Africans
Yoruba
Goun
Mbugu
Sango
Lissongo and
Bagandu
San
Glaokx’ate
Pygmies
Babin ga
Mbuti
Twa
“Western”
Babenga
Blacks
Afro-Jamaicans
Afro-Americans
Djuka
Caucasians’
Ashkenazi Jews
Punjabi Indians
Country
Sample
size
GPX1*2
Cameroon
Congo
Congo
Congo
Rwanda
Rwanda
Botswana
SAR
441
94
79
57
122
16
n.r.
303
0.058
0.058
0.025
0.079
0.045
0.156
0.077
0.058
This study
Destro-Bisol et al. (1987)
Destro-Bisol et al. (1987)
Destro-Bisol et al. (1987)
Meera Khan et al. (1986)
Meera Khan et al. (1986)
Nurse and Jenkins (1977)
Board (1983)
Nigeria
Benin
CAR
CAR
CAR
65
18
32
43
43
0.000
0.028
0.047
0.012
0.093
Ojikutu et al. (1977)
This study
This study
This study
Meera Khan et al. (1986)
Botswana
33
0.000
Nurse and Jenkins (1977)
CAR
Zaire
Rwanda
Cameroon
Congo
927
122
188
18
48
0.005
0.000
0.023
0.000
0.011
Meera Khan et al. (1986)
Meera Khan et al. (1986)
Meera Khan et al. (1986)
Meera Khan et al. (1986)
Destro-Bisol et al. (1987)
Jamaica
USA
Surinam
72
392
715
0.007
0.032
0.054
Meera Khan et al. (1984a)
Beutler et al. (1974)
Meera Khan et al. (1986)
USA
90
0.011
India
116
0.013
Estimated bv Meera Khan et al.
(1984) from Beutler et al. (1974)
Meera Khan et al. (1984a)
Reference
lThe GPXb2 allele was nut found in 110 Norwegians,398 Dutch, and 76 Sardinians(Meera Khan et al., 1984a),300 non-Jewish whites of the
U S A . (estimated by Meera Khan et al., 1984a from Beutler et al., 1974) and 47 Marathi and 198 Telugu of India (Meera Khan et al., 1984a).
As for Amerindians, G P X M was not found in 149 Quechua, 312 Wajana, and 504 Trio Amerindians (Meera Khan et al., 1984a).
222
G. DESTRO-BISOL AND G. SPEDINI
GPXl*2 allele in the HbA and HbAS subsamples of each population (Table 3): the
GPX1*2 was found to be absent in some
HbAS subsamples (Mbugu, Sango, Goun,
Bamileke of Kongsamba and of Ndoungue,
North Bateke, and Babenga), or its frequency
was noticeably lower in others (Bamileke of
Manengole and Beti). Only in the South
Bateke was the GPX1*2 frequency higher
among the HbAS than among the HbA carriers. This group was found to be significantly different from the Babenga and the
Sango with respect to GPXl phenotype distribution (GPX1 2-1 and GPXl 2 2-2 pooled:
GPXl*2 and malaria
South Bateke vs. Babenga xf= 4.547,0.05 > P
Meera Khan et al. (1986) suggested that the > 0.02; South Bateke vs. Sango X ? = 4.104,
GPXl*2 allele product could be less favour- 0.05 > P > 0.02), while no significant differable than the GPX1*1 to the survival of Plas- ences were found among the other population
modium falciparum because of its ability to samples. Interestingly, when the indepenoxidise a higher rate of GSH, a compound dence of GPX1*2 and HbP*S allele distribution
essential for growth and development of the was tested in a 2 X 2 contingency table
P. falciparum parasite. This is a very attrac- (GPX1 2-1 and GPX 2-2 pooled-the South
tive hypothesis. However, the considerably Bateke were excluded owing to their differhigher peroxidasic activity of the GPX1*2 ence in GPXl distribution), a significant
allelic product could have remarkable conse- value was obtained (x?= 7.543, 0.01 > P >
quences on other steps of the biochemical 0.001). These results seem therefore to suppattern of erythrocytes. In the case of the port our hypothesis. However, their value
Subsaharan populations, it would be of par- must be considered with great caution for the
ticular interest to study the possible interac- following reasons: first, this study of interactions between the GPX1*2 allele and the tion between the GPX1*2 allele product and
genetic factors involved in the protection HbAS was performed on too small a scale for
any firm conclusion to be drawn; and second,
against malaria.
Friedman (1981) suggested that the prema- a more faithful evaluation of the occurrence
ture destruction of the red cells infected by of malaria selection on a n association bemalaria parasites in which HbS, or other tween genetic traits requires the simultaneabnormal hemoglobins, are present could be ous investigation of other biochemical polymainly due to reactive species generated by morphisms (e.g., red cell glucose-6-phosphate
the interaction between membrane-bound dehydrogenase) a s well as environmental
abnormal hemoglobins and hydrogen perox- factors (e.g., dietary selenium intake) that
ide excreted by the Plasmodium. It is known could affect the phenotypic expression of the
that GPX1, along with catalase, plays a genetic traits under study and/or the indiprimary role in the elimination of H202 in the vidual resistance to malaria.
In conclusion, our findings support the
red cells (Cohen and Hochstein, 1963), and a
remarkable reduction of GPXl activity could value of GPXl a s a n admixture marker of
be involved in the sickling events (Das and Pygmy with neighbouring Negro populations,
Nair, 1980). Hence, basing our hypothesis on and stimulate us toward further investigathese findings, it seems possible to conclude tions on the existence of an interaction
that the Hbp*S protection against malaria between GPXl*2 and Hb beta*S allelic
might be counteracted by the higher peroxi- products. We have further GPXl studies in
dase activity of the GPXl*2 allelic product. progress, aimed at checking the suggested
The subsequent increase in oxidized gluta- negative association between GPX1*2 and
thione (GSSG) might be counterbalanced by Hbp*S alleles.
a n increased activity of the NADPH/GSSG
reductase system (Wendel, 1980) and/or by
ACKNOWLEDGMENTS
GSSG efflux from erythrocytes (Srivastava
This work was supported by the Minister0
and Beutler, 1969; Sies et al., 1972).
In order to check this speculative hypothe- della Pubblica Istruzione. We are indebted to
sis, we have compared the frequencies of the Prof P. Meera Khan (University of Leiden,
The Babenga have established a gene flow
with the neighboring South Bateke (Spedini
et al., 1985-86), who are characterized by
rather high frequencies of GPX1*2 (0.079;
Destro-Bisol et al., 1986). By supporting the
notion that the presence of GPX1*2 in the
Pygmy group is presumably due to genetic
admixture with neighbouring Negro populations (Meera Khan et al., 1986), our data
allow us to suggest that GPX1*2 could be a
valuable marker in the study of the genetic
admixture between Negro and Pygmy populations.
223
GLUTATHIONE PEROXIDASE IN AFRICA
TABLE 3. Association of GPXl polymorphism with Hbp types
Population
CAR
Mbugu
Sango
Benin
Goun
Cameroon
Bamileke
(Manengole)
(Kongsamba)
(Ndoungue)
Congo
Beti
South Bateke
Babenga
Pooled sample2
Total
GPXl*2
frequency
0
0
0
0
28
4
34
9
0.054
0.000
0.015
0.000
0
0
16
2
0.031
0.000
28
1
1
0
235
21
94
13
70
7
0.064
0.024
0.080
0.000
0.029
0.000
1
63
31
66
13
46
0
0
0
3
0
43
4
650
102
0.079
0.016
0.030
0.000
0.076
0.091
0.012
0.000
0.099
0.001
1-1
A
AS
A
AS
25
4
33
9
3
0
1
0
A
AS
15
2
1
0
A
AS
A
206
20
80
11
66
7
53
30
62
13
40
9
42
4
982
100
10
1
AS
A
AS
A
North Bateke
GPXl phenotype
2-1
2-2
Hbp type’
AS
A
AS
A
AS
A
AS
A
AS
13
0
4
0
4
0
5
2
1
0
65
2
1
0
0
0
0
0
0
0
11
‘The data relative to the Hbp types are reported in Spedini et al. (1983)for the Mbugu and Sango;Spedini et al. (198Ob)for the Goun; Spedini
et al. (1988) for the Bamileke;and Spedini et al. (1986)for the Beti, Bateke, and Babenga.
2The South Bateke were excluded (see text).
The Netherlands) for his help in the interpretation of the unusual GPXl electrotypes, to
Prof. P.G. Board (University of Canberra,
Australia) for providing us with the “Lebanese” variants, and to Dr. A. Briziobello for
his cooperation in GPXl typing.
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