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Hassan et al. Potential antioxidant activity of cape gooseberry against HCC

Table 2: Effect of CGJ administration on oxidative stress and antioxidant biomarkers in liver of control and different
treated rat groups (means ± SE)
Parameters groups MDA (nmol/g) GSH (mg/g) TAC (mmol/L) SOD (U/g) CAT (µmol/s/g)
Control 512.11 ± 0.64 19.46 ± 0.54 95.86 ± 0.03 892.99 ± 1.18 190.73 ± 1.19
CGJ 510.11 ± 0.59 19.99 ± 0.64 97.89 ± 0.13 894.90 ± 1.21 194.73 ± 1.89
HCC 701.80 ± 2.91 a,b 10.06 ± 0.46 a,b 28.11 ± 0.23 a,b 416.99 ± 1.18 a,b 132.55 ± 1.38 a,b
HCC + CGJ 517.11 ± 0.59 c 17.48 ± 0.44 a,b,c 75.47 ± 0.31 a,b,c 841.71 ± 1.77 a,b,c 180.68 ± 1.35 a,b,c
b
c
a P ≤ 0.05 vs. control, P ≤ 0.05 vs. CGJ, P ≤ 0.05 vs. HCC. HCC: hepatocellular carcinoma; CGJ: cape gooseberry juice; MDA:
malondialdehyde; GSH: glutathione; TAC: total antioxidant capacity; SOD: superoxide dismutase; CAT: catalase
Table 3: Effect of CGJ administration on oxidate stress and antioxidant biomarkers in the kidney of control and
different treated rat groups (means ± SE)
Parameters groups MDA (nmol/g) GSH (mg/g) TAC (mmol/L) SOD (U/g) CAT (µmol/s/g)
Control 90.73 ± 1.12 42.56 ± 0.54 72.86 ± 0.23 69.99 ± 0.34 95.56 ± 1.54
CGJ 93.43 ± 1.16 42.99 ± 0.64 77.89 ± 0.13 70.79 ± 0.64 96.99 ± 0.64
HCC 190.93 ± 1.79 a,b 20.06 ± 0.46 a,b 20.21 ± 0.53 a,b 13.49 ± 0.66 a,b 30.16 ± 1.46 a,b
HCC + CGJ 105.77 ± 1.19 a,b,c 29.48 ± 0.44 a,b,c 37.47 ± 0.31 a,b,c 37.48 ± 0.94 a,b,c 70.48 ± 1.44 a,b,c
c
b
a P ≤ 0.05 vs. control, P ≤ 0.05 vs. CGJ, P ≤ 0.05 vs. HCC. HCC: hepatocellular carcinoma; CGJ: cape gooseberry juice; MDA:
malondialdehyde; GSH: glutathione; TAC: total antioxidant capacity; SOD: superoxide dismutase; CAT: catalase
Table 4: Effect of CGJ administration on oxidate stress and antioxidant biomarkers in the brain of control and
different treated rat groups (means ± SE)
Parameters groups MDA (nmol/g) GSH (mg/g) TAC (mmol/L) SOD (U/g) CAT (µmol/s/g)
Control 75.31 ± 0.64 35.46 ± 0.50 75.06 ± 0.13 63.80 ± 0.34 62.43 ± 0.29
CGJ 76.44 ± 0.99 35.99 ± 0.64 77.00 ± 0.12 63.97 ± 0.64 62.43 ± 0.29
HCC 117.80 ± 1.71 a,b 13.76 ± 0.16 a,b 18.25 ± 0.12 a,b 18.25 ± 0.12 a,b 25.58 ± 1.70 a,b
HCC + CGJ 95.71 ± 0.99 a,b,c 23.48 ± 0.24 a,b,c 44.38 ± 0.94 a,b,c 44.38 ± 0.94 a,b,c 48.50 ± 1.05 a,b,c
a P ≤ 0.05 vs. control, P ≤ 0.05 vs. CGJ, P ≤ 0.05 vs. HCC. HCC: hepatocellular carcinoma; CGJ: cape gooseberry juice; MDA:
b
c
malondialdehyde; GSH: glutathione; TAC: total antioxidant capacity; SOD: superoxide dismutase; CAT: catalase
Table 5: Effect of CGJ administration on oxidate stress and antioxidant biomarkers in the testes of control and
different treated rat groups (means ± SE)
Parameters groups MDA (nmol/g) GSH (mg/g) TAC (mmol/L) SOD (U/g) CAT (µmol/s/g)
Control 14.24 ± 0.02 25.02 ± 0.24 76.88 ± 1.23 50.04 ± 0.24 48.94 ± 0.12
CGJ 14.43 ± 0.06 25.28 ± 0.24 77.98 ± 1.13 50.22 ± 0.14 48.97 ± 0.24
HCC 54.96 ± 0.17 a,b 9.06 ± 0.16 a,b 35.55 ± 0.33 a,b 10.41 ± 0.22 a,b 16.03 ± 1.12 a,b
HCC + CGJ 31.95 ± 0.19 a,b,c 19.48 ± 0.04 a,b,c 57.77 ± 0.33 a,b,c 31.52 ± 0.23 a,b,c 30.48 ± 0.44 a,b,c
a b c
P ≤ 0.05 vs. control, P ≤ 0.05 vs. CGJ, P ≤ 0.05 vs. HCC. HCC: hepatocellular carcinoma; CGJ: cape gooseberry juice; MDA:
malondialdehyde; GSH: glutathione; TAC: total antioxidant capacity; SOD: superoxide dismutase; CAT: catalase
the examined tissues; liver, kidney, brain and testis, a good marker for various malignancies including
indicating the antioxidant activity of CGJ [Tables 2-5]. testicular, bile duct, pancreatic, stomach, colon and
hepatic cancer. [36,37] Moreover, the observed elevation
DISCUSSION of serum AST, ALT and ALP and the decrease in
ALT and AST in the liver in HCC rats supports earlier
Recently, there has been growing interest in dietary findings. [38] These findings may be due to damage to
bioactive compounds obtained from natural sources hepatocytes caused by exposure to DENA resulting in
which have a therapeutic effect against various hepatic dysfunction and subsequent leakage of these
diseases including chemoprotective properties against enzymes from the neoplastic cell into circulation. [39]
cancer. [5,33] HCC is a common disease, being the third Or, the findings may be due to the release of enzymes
[34]
leading cause of death worldwide. The current study from normal tissue by tumors or possibly the effect of
suggests that treatment with DENA and CCl 4 is a good tumors on remote tissue, leading to leakage of enzyme
model for the induction of HCC in rats. [35] The data and release into the blood. [40] In a related concern it has
also showed increased AFP in HCC rats. Increase been suggested that there is an increase in the levels of
of this protein may be due to hepatotoxic agents or these transaminases activity in serum of HCC patients.
hepatocarcinogens that are frequently associated with
HCC. Increased glycoprotein AFP levels is considered In concurrence with the above findings, elevated serum
30 Hepatoma Research ¦ Volume 3 ¦ February 28, 2017