References
211. Serum selenium, plasma
glutathione (GSH) and erythrocyte glutathione
peroxidase (GSH?Px)?levels in asymptomatic versus
symptomatic human
immunodeficiency virus?1 (HIV?1)?infection.
Look MP, Rockstroh JK, Rao GS, Kreuzer KA, Barton S, Lemoch
H, Sudhop T, Hoch J, Stockinger K, Spengler U, Sauerbruch
T
Department of General Internal Medicine, University of Bonn,
Germany.
Eur J Clin Nutr. 1997 Apr;51(4):266-72.
OBJECTIVES: Antioxidant defense status was investigated in
HIV?infected patients by measuring serum selenium,
erythrocyte glutathione peroxidase (GSH?Px) activity, plasma
thiol (?SH) and glutathione (GSH) concentrations along with
the assessment of the clinical stage and surrogate markers of
HIV?disease. DESIGN, SETTING AND SUBJECTS: Serum selenium
levels were determined cross?sectionally in 104 sequentially
selected HIV?infected patients (83 outpatients and 21
patients with ongoing AIDS defining events). The patients
were classified into three stages of the disease, I, II and
III according to the 1993 Centers For Disease Control (CDC)
classification system for HIV?infection. GSH?Px activities,
plasma SH and plasma GSH concentrations were determined in a
subset of 24 patients at stage I and 12 patients at stage III
with an active AIDS?defining disease. RESULTS: Mean serum
selenium levels were lower in CDC stage II (68.7 +/? 20.9
micrograms/l; P < 0.01; n = 34) and stage III (51.4 +/?
14.7 micrograms/l; P < 0.01; n = 37) HIV?infected patients
than in healthy subjects (89.2 +/? 20.9 micrograms/l; n = 72)
and stage I patients (82.3 +/? 20.5; microgram/l; n = 33).
Serum selenium levels were positively correlated with
CD4?count (r = 0.42; P < 0.001; n = 104) and inversely
with levels of soluble tumor necrosis factor receptors type
II (r = ?0.58; P < 0.01; n = 35), neopterin (r = ?0.5; P
< 0.001; n = 80) and beta 2?microglobulin (r = ?0.4; P
< 0.001; n = 94). Hepatitis C virus (HCV) and
HIV?coinfected patients at CDC stages I and II showed
markedly lower selenium concentrations compared to
HIV?infected patients without concomitant HCV?infection.
Serum selenium and GSH?Px activity in hospitalized AIDS
patients was significantly lower as compared to asymptomatic
patients and healthy subjects, whereas plasma SH and GSH
concentrations were lower in both, asymptomatic ?and
AIDS?patients, than in the controls. CONCLUSION: The results
show that stages I?III of HIV?disease are characterized by
significant impairments of antioxidative defenses provided by
selenium, GSH?Px, SH?groups and GSH.
212. Micronutrient levels in
HIV?1?infected children.
Periquet BA; Jammes NM; Lambert WE; Tricoire J; Moussa MM;
Garcia J; Ghisolfi J; Thouvenot J
Purpan Hospital, Toulouse, France.
AIDS, 1995 Aug, 9:8, 887?93
OBJECTIVE: Micronutrients (zinc, copper, selenium, vitamin
A, E, and carotenoids) are essential for the integrity of
host defences. This study was designed to determine the
prevalence of abnormalities of the micronutrient levels in
HIV?1?seropositive children. DESIGN: Prospective study.
SETTING: The study was performed on HIV?1?infected children
at the Paediatric Haematology and Oncology Unit of Toulouse
Hospital, France. PATIENTS: Twenty?one children, suffering
from HIV?1 infection and 21 control subjects of similar age
(2?9 years) were included in the study. In the HIV?1?infected
children, two subgroups were considered according to stage
(non?AIDS or AIDS), based on the Centers for Disease Control
and Prevention 1987 criteria. RESULTS: The first
statistically significant deficiencies occurred at non?AIDS
stage and were confirmed at AIDS stage: P < 0.05 for
lycopene, retinol, tocopherol and P < 0.001 for
transthyretin and serum albumin. Levels of copper (40%) and
long?chain polyunsaturated fatty acids (21%) were higher in
the non?AIDS group than the controls. CONCLUSION: Biological
impairing of the micronutrient levels was observed in the
non?AIDS stage without clinical sign. This information is
useful in delineating eventual and well considered
nutritional intervention strategies that may improve the
clinical status of HIV?1?infected children and perhaps alter
the course of their disease.
213. Selenium supplementation
suppresses tumor necrosis factor alpha?induced human
immunodeficiency virus type 1 replication in vitro.
Hori K; Hatfield D; Maldarelli F; Lee BJ; Clouse KA
Division of Cytokine Biology, Center for Biologics
Evaluation and Research, Food and Drug Administration,
Rockville, Maryland 20852, USA.
AIDS Res Hum Retroviruses, 1997 Oct, 13:15, 1325?32
Selenium is a nutritionally essential trace element that is
important for optimal function of the immune system. It is
incorporated into selenoproteins as the amino acid
selenocysteine and it is known to inhibit the expression of
some viruses. In this study, we show that selenium
supplementation for 3 days prior to exposure to tumor
necrosis factor alpha (TNF?alpha) partially suppresses the
induction of human immunodeficiency virus type 1 (HIV?1)
replication in both chronically infected T lymphocytic and
monocytic cell lines. In acute HIV?1 infection of T
lymphocytes and monocytes in the absence of exogenous
TNF?alpha, the suppressive effect of selenium supplementation
was not observed. However, selenium supplementation did
suppress the enhancing effect of TNF?alpha on HIV?1
replication in vitro in acutely infected human monocytes, but
not in T lymphocytes. Selenium supplementation also increased
the activities of the selenoproteins, glutathione peroxidase
(GPx) and thioredoxin reductase (TR), which serve as cellular
antioxidants. Taken together, these results suggest that
selenium supplementation may prove beneficial as an adjuvant
therapy for AIDS through reinforcement of endogenous
antioxidative systems.
214. natural antimutagenic
agents may prolong efficacy of human immunodeficiency virus
drug therapy.
McCarty MF
Nutrition 21, San Diego, CA 92109, USA.
Med Hypotheses, 1997 Mar, 48:3, 215?20
The long?term efficacy of new combination drug therapies for
human immunodeficiency virus infection may be limited by the
tendency of transfected human immunodeficiency virus to
mutate to drug?resistant forms. This argues for the use of
safe antimutagenic measures as adjuvants to such therapies.
Certain nutrients and food factors?notably selenium,
green?tea polyphenols, and cruciferous phytochemicals?can
suppress cancer initiation and mutagenesis in animal and cell
culture models; epidemiological studies suggest that ambient
variations in consumption of these food factors can have an
important impact on human cancer rates. Low?fat diets may
reduce deoxyribonucleic acid base damage in human leukocytes,
whereas increased body iron stores are
likely to increase mutation rates. Thus, ample but safe
intakes of selenium, green?tea
polyphenols, and cruciferous vegetables, in the context of a
diet low in fat and assimilable iron, can be expected to
prolong the efficacy of drug therapy in subjects infected
with the human immunodeficiency virus. These measures can
also be recommended for cancer prevention in the general
population
215. Serum selenium
concentration and disease progress in patients with HIV
infection.
Cirelli A; Ciardi M; de Simone C; Sorice F; Giordano R;
Ciaralli L; Costantini S
Istituto Malattie Infettive, University La Sapienza, Rome,
Italy.
Clin Biochem, 1991 Apr, 24:2, 211?4
The selenium concentration in the serum of 67 patients with
HIV infection was measured to determine whether selenium
deficiency occurred in the different stages of the disease.
In the first stage of the study, patients were divided into
four groups: symptom?free subjects, PGL (persistent
generalized lymphadenopathy), ARC (AIDS related complex), and
AIDS (acquired immunodeficiency syndrome). Selenium
concentrations were normal in HIV antibody positive
symptom?free subjects (1.18 +/? 0.27 mumol/L) and lower than
normal in the other three groups (p less than 0.001). There
was a significant correlation (p less than 0.001) between
selenium levels and values of hemoglobin and erythrocyte
sedimentation rate. Selenium deficiency was in no case
associated with a lack of zinc in serum (also determined in
all patients). In the second stage of the study, 12 patients
were treated for a period of two months with low doses of
selenium to assess whether such supplementation was able to
restore their impaired immunological and hematological
functions. The therapy increased serum selenium
concentrations (from 0.77 +/? 0.23 to 1.44 +/? 0.41 mumol/L)
and symptomatic improvements were noted. However, no changes
were observed in the immunological and hematological
parameters.
216. Serum selenium, plasma
glutathione (GSH) and erythrocyte glutathione
peroxidase
(GSH?Px)?levels in asymptomatic versus symptomatic human
immunodeficiency virus?1
(HIV?1)?infection.
Look MP; Rockstroh JK; Rao GS; Kreuzer KA; Barton S; Lemoch
H; Sudhop T; Hoch J;
Stockinger K; Spengler U; Sauerbruch T
Department of General Internal Medicine, University of Bonn,
Germany.
Eur J Clin Nutr, 1997 Apr, 51:4, 266?72
OBJECTIVES: Antioxidant defense status was investigated in
HIV?infected patients by measuring serum selenium,
erythrocyte glutathione peroxidase (GSH?Px) activity, plasma
thiol (?SH) and glutathione (GSH) concentrations along with
the assessment of the clinical stage and surrogate markers of
HIV?disease. DESIGN, SETTING AND SUBJECTS: Serum selenium
levels were determined cross?sectionally in 104 sequentially
selected HIV?infected patients (83 outpatients and 21
patients with ongoing AIDS defining events). The patients
were classified into three stages of the disease, I, II and
III according to the 1993 Centers For Disease Control (CDC)
classification system for HIV?infection. GSH?Px activities,
plasma SH and plasma GSH concentrations were determined in a
subset of 24 patients at stage I and 12 patients at stage III
with an active AIDS?defining disease. RESULTS: Mean serum
selenium levels were lower in CDC stage II (68.7 +/? 20.9
micrograms/l; P < 0.01; n = 34) and stage III (51.4 +/?
14.7 micrograms/l; P < 0.01; n = 37) HIV?infected patients
than in healthy subjects (89.2 +/? 20.9 micrograms/l; n = 72)
and stage I patients (82.3 +/? 20.5; microgram/l; n = 33).
Serum selenium levels were positively correlated with
CD4?count (r = 0.42; P < 0.001; n = 104) and inversely
with levels of soluble tumor necrosis factor receptors type
II (r = ?0.58; P < 0.01; n = 35), neopterin (r = ?0.5; P
< 0.001; n = 80) and beta 2?microglobulin (r = ?0.4; P
< 0.001; n = 94). Hepatitis C virus (HCV) and
HIV?coinfected patients at CDC stages I and II showed
markedly lower selenium concentrations compared to
HIV?infected patients without concomitant HCV?infection.
Serum selenium and GSH?Px activity in hospitalized AIDS
patients was significantly lower as compared to asymptomatic
patients and healthy subjects, whereas plasma SH and GSH
concentrations were lower in both, asymptomatic ?and
AIDS?patients, than in the controls. CONCLUSION: The results
show that stages I?III of HIV?disease are characterized by
significant impairments of antioxidative defenses provided by
selenium, GSH?Px, SH?groups and GSH.
217. Selenium and HIV
infection [editorial]
Constans J; Conri C; Sergeant C
Nutrition, 1999 Sep, 15:9, 719?20
Abstract unavailable online.
218. Selenium supplementation
of symptomatic human immunodeficiency virus infected
patients.
Olmsted L; Schrauzer GN; Flores Arce M; Dowd J
Department of Family Medicine, School of Medicine,
University of California, San Diego, La Jolla 92093.
Biol Trace Elem Res, 1989 Apr, 20:1?2, 59?65
The mean whole blood selenium levels in male San Diego, CA
patients with acquired immune deficiency syndrome (AiDS) are
0.123 +/? 0.030 micrograms/mL (n = 24), and 0.126 +/? 0.038
micrograms/mL (n = 26) in patients with AIDS?related complex
(ARC), compared to 0.195 +/?0.020 micrograms/mL (n = 28) in
San Diego healthy controls (males). To establish whether
intestinal absorption of dietary selenium is impaired in AIDS
or ARC, a supplementation trial was conducted in which 19
symptomatic HIV?antibody positive male patients with AIDS or
ARC were taking 400 micrograms of selenium/d in form of
selenium yeast for up to 70 d. The mean whole blood Se levels
increased to 0.28 +/? 0.08 micrograms/mL after 70 d of
supplementation, the selenium supplements were well
tolerated. A rationale for adjuvant selenium supplementation
of symptomatic and asymptomatic HIV carriers is proposed.
219. Genomic structures of
viral agents in relation to the biosynthesis of
selenoproteins.
Taylor EW; Nadimpalli RG; Ramanathan CS
Computational Center for Molecular Structure and Design,
University of Georgia, Athens
30601?2352, USA. wtaylor@rx.uga.edu
Biol Trace Elem Res, 1997 Jan, 56:1, 63?91
The genomes of both bacteria and eukaryotic organisms are
known to encode selenoproteins, using the UGA codon for
seleno?cysteine (SeC), and a complex cotranslational
mechanism for SeC incorporation into polypeptide chains,
involving RNA stem?loop structures. These common features and
similar codon usage strongly suggest that this is an ancient
evolutionary development. However, the possibility that some
viruses might also encode selenoproteins remained unexplored
until recently. Based on an analysis of the genomic structure
of the human immunodeficiency virus HIV?1, we demonstrated
that several regions overlapping known HIV genes have the
potential to encode selenoproteins (Taylor et al. [31], J.
Med. Chem. 37, 2637?2654 [1994]). This is provocative in the
light of overwhelming evidence of a role for oxidative stress
in AIDS pathogenesis, and the fact that a number of viral
diseases have been linked to selenium (Se) deficiency, either
in humans or by in vitro and animal studies. These include
HIV?AIDS, hepatitis B linked to liver disease and cancer,
Coxsackie virus B3, Keshan disease, and the mouse mammary
tumor virus (MMTV), against which Se is a potent
chemoprotective agent. There are also established biochemical
mechanisms whereby extreme Se deficiency can induce a
proclotting or hemorrhagic effect, suggesting that
hemorrhagic fever viruses should also be examined for
potential virally encoded selenoproteins. In addition to the
RNA stem?loop structures required for SeC insertion at UGA
codons, genomic structural features that may be required for
selenoprotein synthesis can also include ribosomal frameshift
sites and RNA pseudoknots if the potential selenoprotein
module overlaps with another gene, which may prove to be the
rule rather than the exception in viruses. One such
pseudoknot that we predicted in HIV?1 has now been verified
experimentally; a similar structure can be demonstrated in
precisely the same location in the reverse transcriptase
coding region of hepatitis B virus. Significant new findings
reported here include the existence of highly distinctive
glutathione peroxidase (GSH?Px)?related sequences in
Coxsackie B viruses, new theoretical data related to a
previously proposed potential selenoprotein gene overlapping
the HIV protease coding region, and further evidence in
support of a novel frameshift site in the HIV nef gene
associated with a well?conserved UGA codon in the 1?reading
frame.
220. Clin Chim Acta 1994 Oct
14;230(1):35-42
Vitamin, trace element and peroxide status in HIV
seropositive patients:
asymptomatic patients present a severe beta-carotene
deficiency.
Sappey C, Leclercq P, Coudray C, Faure P, Micoud M, Favier
A
Groupe de Recherche et d'etude sur les Pathologies
Oxydatives (GREPO), Faculte de
Medecine et de Pharmacie, La Tronche, France.
We have investigated whether nutritional status and
peroxidation process are associated with the degree of
development of HIV infection. This was done by measuring the
status of vitamins (E, A and beta-carotene), of antioxidant
trace elements (zinc, selenium) and lipid peroxide levels
(lipid hydroperoxides and thiobarbituric acid reactants) in
HIV-seropositive patients at CDC II and CDC IV stages and in
comparison with normal subjects. There was a decrease in
vitamin and trace element levels related to the severity of
disease. The most dramatic decrease, however, was seen for
carotenoids (0.94 +/- 0.46 mumol/l) and beta-carotene (0.24
+/- 0.14 mumol/l vs. 0.56 +/- 0.29 mumol/l) whose stage II
levels were only half the normal value. Paradoxically, lipid
peroxidation was higher at stage II than at stage IV. This
can be attributed to an overproduction of oxygen radicals by
polymorphonuclears in stage II. This deficiency in
antioxidant status, often found in patients suffering from
peroxidative diseases, may have
important consequences on cellular immunity. Furthermore,
the concomitant overproduction of free radicals may also
affect HIV multiplication.