has been abbreviated unchanged from the original document
except for the bold emphasis editing by Stuart Thomson,
Director, the Gaia Research Institute. S.T.) (We are keen
to determine whether this research has been taken into
consideration by the Medicines Control Council in its
recent re-endorsement of this deadly toxic agent. S.T.)
Toxicology and Carcinogenesis Studies of AZT (CAS No.
30516-87-1) and AZT/a-Interferon A/D B6C3F1 Mice (Gavage
3'-Azido-3'-deoxythymidine (AZT) is the
most widely used and evaluated chemotherapeutic agent
for the treatment of persons with acquired immune deficiency
syndrome (AIDS) and persons seropositive for human immunodeficiency
virus (HIV). The National Cancer Institute nominated
AZT for toxicity and carcinogenicity studies because of
the impending large-scale use of AZT in the treatment
of adult patients with AIDS or AIDS-related complex.
Exposure to AZT was toxic
to the bone marrow, resulting in significant changes in
the peripheral blood (decreased hematocrit values, erythrocyte
counts, and hemoglobin concentrations, and increased mean
cell volume and mean cell hemoglobin) and bone marrow
(erythroid hypoplasia) characteristic of a dose- and time-dependent,
minimal to moderate, poorly regenerative macrocytic anemia.
and Bone Marrow Analyses
All groups of male and
female mice receiving AZT exhibited changes in peripheral
blood and bone marrow characteristic of a dose- and time-dependent,
minimal to mild, macrocytic, nonresponsive anemia. In
females, these changes were evident throughout the study.
In males, the macrocytic anemia had resolved by week 80
in the 30 mg/kg group; at study termination erythrocyte
macrocytosis was present only in males receiving 60 or
120 mg/kg AZT.
Incidences of squamous
cell carcinoma and squamous cell papilloma or carcinoma
(combined) of the vagina occurred with a positive trend
and were significantly increased in groups of female mice
receiving 60 or 120 mg/kg AZT. Epithelial hyperplasia
was observed in all dosed groups of females, and the incidence
was significantly increased in the 120 mg/kg AZT group.
Three renal tubule adenomas and
one renal tubule carcinoma were observed in male mice
receiving 120 mg/kg AZT; the combined incidence in this
group exceeded the range in historical controls. Evaluation
of step sections revealed a few more renal tubule hyperplasias.
The incidence of harderian gland
adenoma was increased in male mice receiving 120 mg/kg
AZT and exceeded the range in historical controls.
AZT is mutagenic in vitro
and in vivo. It induced gene mutations in Salmonella
typhimurium strain TA102. AZT induced sister chromatid
exchanges in cultured Chinese hamster ovary cells. In
vivo studies with male mice administered AZT by gavage
showed highly significant increases in micronucleated
erythrocytes in bone marrow and peripheral blood after
exposure periods that ranged from 72 hours to 14 weeks.
Under the conditions of
these 2-year gavage studies there was equivocal evidence
of carcinogenic activity of AZT in male mice based on
increased incidences of renal tubule and harderian gland
neoplasms in groups receiving AZT alone. There was clear
evidence of carcinogenic activity of AZT in female mice
based on increased incidences of squamous cell neoplasms
of the vagina in groups that received AZT.
in all groups that received AZT.
Treatment with AZT resulted
in increased incidences of epithelial hyperplasia of the
vagina in all dosed groups of females.
Synonyms: AZT; 3'-azido-2',3'-dideoxythymidine;
azidodeoxythymidine; azidothymidine; 3'-azidothymidine;
3'-deoxy-3'-azidothymidine; 3'-deoxy-(8CI) (9CI); BW A509U;
Compound S; ZDV; zidovudine
Trade name: Retrovir®
Report Date: February 1999
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Preliminary data has for several years indicated that
AZT represented unacceptable risks. Responsible scientists
accordingly called for comprehensive testing such as that
reported above, which is always mandatory prior to the
approval of all other drugs before licensing. AZT (as
is Fluoride) is unique in that it alone was approved for
“human experimentation” prior to such animal
studies having been conducted, and this for the treatment
of a disease of widely scientifically disputed etiology.
Existing pro-AZT studies are fraudulent in that they have
been subject to serious methodological flaws and or were
strategically terminated prematurely, prior to the drug
revealing it’s true unacceptable risk / benefit
profile and the paradoxical inevitable suppression of
immunity, not similarly prevented by experimental termination
in real-life applications of this drug. For insight into
the fraudulent trials see: http://www.virusmyth.net/aids/data/jlfraud.htm