| ORIGINAL ARTICLE |
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The experiment
focused on the endocrinological, histopathological and biochemical
effects of a Cannabis extract (CAN) containing cannabinoids from
Cannabis sativa on the male reproductive system of mammals. The
experiment involved five groups of albino mice (FBV/N strain), with 12
mice in each group. The groups were labeled as follows: CV-I, a control
group treated with alcohol vehicle; CAN-II, a group treated with
40mg/mouse of CAN; CAN-III, a group treated with 60mg/mouse of CAN;
CAN-IV, a group treated with 80mg/mouse of CAN; and CAN-V-R, a
withdrawal group allowing for a 45-day recovery period after receiving
80mg/mouse of CAN treatment. The experimental subjects were given CAN
through intraperitoneal injection.
At low doses (40mg/mouse and 60mg/mouse), significant histopathological
changes were observed, including a reduction in the weight of the
testes, seminal vesicle, and epididymis, shrinkage of seminiferous
tubules, impairment of the spermatogenic cycle, and a reduction in
sperm count. There were also significant changes in protein, lipid, and
cholesterol content, as well as in the concentration of steroidogenic
enzymes such as 3-β hydroxysteroid dehydrogenase (3β-HSD), 17-β
hydroxysteroid dehydrogenase (17β-HSD), testicular acetylcholinesterase
(tACHE), and testicular angiotensin-converting enzyme (tACE) at low
doses. The reduction of 3β-HSD and 17β-HSD at low doses also affected
the concentration of serum testosterone, supporting the higher value of
cholesterol content. Additionally, a reduction in gonadotropins (FSH
and LH) at low doses was documented, along with hypertrophied pituitary
due to positive feedback stimulation. The reduction of lipid content
was likely related to lipid peroxidation due to an increase in the
amount of conjugated dienes.
However, in the high-dose group (80mg/mouse) and the withdrawal group
(CV-V-R), gradual recovery in all parameters was observed. In
conclusion, it is suggested that high-dose CAN treatment produces a
sort of stress that likely activates some stress-induced genes
responsible for minimizing the drastic effects of CAN produced by
low-dose treatment.
