The influence of active hexose correlated compound (AHCC) on cisplatin-evoked chemotherapeutic and side effects in tumor-bearing

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Toxicol
Appl Pharmacol.
2007 Jul 15;222(2):152-8. Epub 2007 Apr 20.
The
influence of active hexose correlated compound (AHCC) on
cisplatin-evoked chemotherapeutic and side effects in tumor-bearing
mice.

Hirose
A
, Sato
E
, Fujii
H
, Sun
B
, Nishioka
H
, Aruoma
OI
.
Amino Up Chemical Company, 363-32 Shin-ei,
Kiyota-ku, Sapporo 004-0839, Japan.

Cisplatin
(cis-diaminedichloroplatinum (II) or CDDP) (a widely used
platinum-containing anticancer drug) is nephrotoxic and has a low
percentage of tolerance in patients during chemotherapy. The active
hexose correlated compound (AHCC) is an extract of Basidiomycotina
marketed as a supplement for cancer patients due to its nutrients and
fibre content and its ability to strengthen and optimize the capacity of
the immune system. The possibility that AHCC could reduce the side
effects of cisplatin was assessed in the tumor-bearing BALB/cA mice on
the basis of the ability to ameliorate the cisplatin-induced body weight
loss, anorexia, nephrotoxicity and hematopoietic toxicity. Although
cisplatin (8 mg/kg body weight) reduced the size and weight of the solid
tumors, supplementation with AHCC significantly enhanced
cisplatin-induced antitumor effect in both the size (p<0.05) and
weight (p<0.05). Food intake in the cisplatin-treated mice were
decreased following commencement of treatment and this remained low
compared with the cisplatin-untreated group (control) throughout the
experiment period. Supplementation with AHCC increased the food intake
in the cisplatin-treated mice. The blood urea nitrogen and serum
creatinine concentrations, and the ratio of blood urea nitrogen to serum
creatinine were significantly increased in the cisplatin alone treated
group compared to the control group. Their increased levels were
mitigated by supplementation with AHCC (100 mg/kg body weight) in the
cisplatin-treated group. AHCC was also able to modulate the suppression
of bone marrow due to cisplatin and the improvement was statistically
significant. The histopathological examination of the kidney revealed
the presence of cisplatin-induced damage and this was modulated by AHCC
treatment. The potential for AHCC to ameliorate the cisplatin-evoked
toxicity as well as the chemotherapeutic effect could have beneficial
economic implications for patients undergoing chemotherapy with
cisplatin.