34
Preclinical evidence
P R O B E
• V o l . L I I I • N o . 3 • A p r – J u n 2 0 1 4
Mitra SK, et al.
Effect of Cystone on Glycolic Acid-induced Uroliathiasis
be due to the ready conversion of
glycolic acid to oxalate by the oxalate
synthesizing liver enzyme glycolate
oxidase. Hyperoxaluria is usually the
initiating factor of oxalate urolithiasis.
Glyolic acid, the precursor of oxalic
acid, is known to significantly
increase the incidence of oxalate
lithiasis. Our results are in agreement
with these studies, as shown by the
significant increase in kidney weight.
The increase in urinary calcium
and oxalate levels were also found
to be highly significant. Cystone
treatment at a dosage of 250, 500,
and 750 mg/kg body weight revealed
a dose-related response. Cystone
treatment at dose levels of 500 and
750 mg/kg body weight showed a
better protective effect. However, there
was no significant difference observed
between 500 and 750 mg/kg body
weight of Cystone treatment.
These findings revealed that 500
mg/kg body weight of Cystone is the
minimum dose required for eliciting
an optimal activity. Cystone treatment
significantly lowered the oxalate values
(
P
< .01) probably by its inhibitory
action on glycolate oxidase. Urinary
sodium excretion was significantly
elevated in the drug-treated animals.
Urinary potassium excretion was also
elevated, though not significantly
(Table 1). The reduction in the urinary
oxalate level will be beneficial in
preventing the urinary supersaturation
with respect to oxalate. Calcium and
phosphorus play a vital role in renal
calculogenesis. Calcium and inorganic
phosphorus levels were also elevated in
the rats receiving a calculi-producing
diet. The increase in calcium excretion
may be due to defective tubular
reabsorption in the kidneys. Cystone
treatment markedly reduced the levels
of calcium and phosphorus (
P
< .01) in
urine (Table 1).
There was a significant increase in the
kidney weight of animals receiving
3% glycolic acid, which was almost
normalized in the Cystone-treated
animals (Table 2). Glycolic acid
feeding for 42 days resulted in renal
tissue deposition of calcium and
oxalate. The increased deposition
of calcium and oxalate in the renal
tissue is known to lead to papillary
calcification and eventual calculi
formation. A similar elevation in renal
stone-forming constituents in rats fed
with CPD has been reported earlier.
Cystone administration significantly
reduced both calcium and oxalate
levels in kidneys, which is known to
prove beneficial in preventing calculi
formation due to supersaturation of
these lithogenic substances (Table 2).
The reduction in the stone forming
constituents in urine and renal
tissue brought about by Cystone
treatment in calculosis is noteworthy.
These effects could contribute to the
antilithic and lithotriptic properties of
this formulation.
