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Table 1: Effect of DADS administration on animal survival percent EAC-aliquot volume, EAC-cells number and percent of
dead cells in EAC-bearing mice
Groups Animal survival EAC-aliquot Total EAC-cell EAC-aliquot volume/ Alive EAC-cell Dead EAC-cell Percent of
7
7
7
percent (%) volume (mL) number (×10 ) total EAC-number (%) number (×10 ) number (×10 ) dead EAC-cells
EAC-bearing mice 66.66 6.56 ± 0.49 121.31 ± 14.13 5.41 ± 0.63 118.33 ± 13.64 2.71 ± 0.23 2.38 ± 0.19
control (n = 8)
EAC-bearing 83.33 4.90 ± 0.19** 51.81 ± 4.24** 9.46 ± 0.61** 48.09 ± 4.27** 3.72 ± 0.19** 7.61 ± 0.98**
mice treated with
DADS (n = 10)
F-probability - P < 0.01 P < 0.001 P < 0.001 P < 0.001 P < 0.01 P < 0.001
LSD at the 5% level - 1.027 28.45 2.51 27.62 0.63 2.38
LSD at the 1% level - 1.416 39.20 3.64 38.05 0.86 3.28
Data are expressed as mean ± SE. **P < 0.01: effect is highly signifi cant; difference between two means of the same parameter is higher than the value of LSD at
the 1% level. EAC: Ehrlich ascites carcinoma; DADS: diallyl disulfi de; LSD: least signifi cance difference; SE: standard error

Table 2: Effect of DADS administration on plasma and ascites sialic acid concentration in EAC-bearing mice
Groups Plasma sialic acid Percent change Ascites sialic acid Percent change
concentration (mg/100 mL) concentration (mg/g protein)
EAC-bearing mice control (n = 8) 91.72 ± 1.26 241.59 ± 11.77
EAC-bearing mice treated with DADS (n = 10) 59.57 ± 4.99** -35.05 172.74 ± 4.72** -28.49
F-probability P < 0.001 P < 0.001
LSD at the 5% level 12.13 24.84
LSD at the 1% level 16.71 34.23
Data are expressed as mean ± SE. **P < 0.01: difference is highly signifi cant; difference between two means is higher than value of LSD at the 5% level. EAC: Ehrlich
ascites carcinoma; DADS: diallyl disulfi de; LSD: least signifi cance difference; SE: standard error

After noticing that DADS induces EAC-apoptosis, the changes
in anti-apoptotic protein Bcl-2 and pro-apoptotic mediator
p53 as well as DNA fragmenting marker TdT were followed
to determine the mechanism of EAC killing.

As indicated in Figure 2, the treatment of EAC-bearing
a b
mice with DADS induced a potential decrease of Bcl-2
expression (yellowish brown color) in the cytoplasm of
EAC-cells [Figure 2b] as compared to the control [Figure 2a]. In
contrast, p53 protein concentration was noticeably increased
in the cytoplasm and nuclei of EAC-cells of DADS-treated
mice [Figure 2d] as compared to the control [Figure 2c].
Similarly, TdT expression was remarkably increased in the
nuclei of EAC-cells in DADS-treated mice [Figure 2f] as
c d compared with the control counterpart [Figure 2e].
Figure 1: Photomicrographs of HE stained EAC-cells sections showing
decreased number of cells, plasma membrane blebbing (mb), fragmenting Data of imaging and semi-quantitative analysis
nuclei (fn), chromatin compaction or condensation (cc), apoptotic bodies (ap) Imaging and semi-quantitative analysis results are represented
and extracellular exudates (ee) (b, ×100; d, ×1000), as a result of treatment
of EAC-bearing mice with DADS as compared to EAC-bearing control mice in Figures 3 and 4.
(a, ×100; c, ×1000) which have EAC-cells with bigger size, abundant basophilic
cytoplasm (bc), and moderate sized-nuclei. EAC: Ehrlich ascites carcinoma; Photomicrographs obtained from imaging analysis depicted
DADS: diallyl disulfi de
that the amount of expressed Bcl-2 has clearly decreased
light stained eosinophilic cytoplasm with azurophilic lytic in EAC-bearing mice treated with DADS [Figure 3b]
bodies. Many EAC-cells, after treatment with DADS, exhibited as compared to EAC-bearing control mice [Figure 3a].
apoptotic signs including shrinkage, blebbing plasma On the other hand, the expressed p53 [Figure 3d] and
membrane, apoptotic bodies, nuclear chromatin compaction, TdT [Figure 3f] are much higher in EAC-bearing mice treated
and fragmenting nuclei. Between EAC-cells, there was a large with DADS than in those of the corresponding EAC-bearing
amount of eosinophilic material or exudates. controls [Figure 3c and e].

70 Hepatoma Research | Volume 1 | Issue 2 | July 15, 2015