1. Volume 8, Issue 3, Pages 205-214 (June 2002)
α-Tocopheryl-l-ascorbate-2-O-phosphate diester, a hydroxyl radical scavenger, prevents the occurrence of epileptic foci in a rat model of post-traumatic epilepsy 
Nihei Yamamoto, Hideaki Kabuto, Sigekiyo Matsumoto, Norio Ogawa, Isao Yokoi 
Pathophysiology 
Volume 8, Issue 3, Pages (June 2002)
DOI: /S (02)

2. Fig. 1
Chemical structure of EPC-K1. EPC-K1: l-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2(4,8,12-trimethyl-tridecyl)-2H-1-benzopyran-6yl-hydrogen phosphate] potassium salt (molecular weight: 706.9).
Pathophysiology 2002 8, DOI: ( /S (02) )

3. Fig. 2
Effect of EPC-K1 on TBARS formation in rat brain homogenate. Rat brain homogenate was incubated with 100 μM of FeCl3 and EPC-K1 for 20 min. TBARS formation induced by FeCl3 was significantly decreased by supplementing with 10 μM of EPC-K1. Mean±S.E.M. (N=6) and *P<0.05.
Pathophysiology 2002 8, DOI: ( /S (02) )

4. Fig. 3
Effect of EPC-K1 on P-Carb formation in rat brain homogenate. Rat brain homogenate was incubated with 10 μM of FeCl3 and EPC-K1 for 15 min. P-Carb formation induced by FeCl3 was significantly decreased by supplementing with 0.10 μM of EPC-K1. Mean±S.E.M. (N=6) and *P<0.05.
Pathophysiology 2002 8, DOI: ( /S (02) )

5. Fig. 4
Effect of EPC-K1 on the development of seizure activity induced by FeCl3 in acute experiments. Left column: 5 μl of FeCl3 solution (100 mM) was injected into the motor cortex. In the middle ECoGs, spike bursts appear in the LF 59 min after the injection, and in the lower ECoGs epileptiform discharges in all leads 182 min after the injection. Right column: 5 μl of EPC-K1 (0.1 mM) dissolved in FeCl3 solution (100 mM) was injected, there was no spike activity 60 and 180 min after the injection. The recordings were performed by four epidural electrodes and ECG (electrocardiogram). Positions of electrodes and the drug injection site are shown in the lowest right corner.
Pathophysiology 2002 8, DOI: ( /S (02) )

6. Fig. 5
Occurrence of epileptiform discharges in ECoGs after FeCl3 injection into the rat motor cortex. Each rat was injected with 5 μl of EPC-K1 dissolved in FeCl3 solution (100 mM) into the motor cortex. Five microliters contained 0–5 nmol of EPC-K1. Ordinate, percent induction of epileptiform discharges; and abscissa, time after the injection.●, FeCl3 (500 nmol) without EPC-K1; ○, FeCl3 with 5 pmol of EPC-K1; ■, FeCl3 with 25 pmol of EPC-K1; □, FeCl3 with 100 pmol of EPC-K1; ▴, FeCl3 with 250 pmol of EPC-K1; ▵, FeCl3 with 500 pmol of EPC-K1; ♦, FeCl3 with 2.5 nmol of EPC-K1; and ♢, FeCl3 with 5 nmol of EPC-K1. *P<0.05 compared with 0 pmol of EPC-K1 by the Fischer's exact test.
Pathophysiology 2002 8, DOI: ( /S (02) )

7. Fig. 6
Changes in diet intake in the four experimental groups. Four groups of rats ate almost the same amount of diet, and EPC-K1 uptake was calculated to 80 mg/kg/day. Ordinate, solid number is diet intake (g/kg/day), and italic number is EPC-K1 intake (mg/kg/day); and abscissa, weeks after the injection. In each group, 13 (0–17 weeks) and seven rats (18–27 weeks) were used. Standard deviations at each point were within 7% of mean value. ○, HCl+CE group; □, HCl+EPC group; ●, Fe+CE group; and ■, Fe+EPC group.
Pathophysiology 2002 8, DOI: ( /S (02) )

8. Fig. 7
Changes in body weight in the four experimental groups. Among the four groups, the growth rate of FeCl3-injected rats with standard diet (Fe+CE group) was poor, however, EPC-K1 supplemented into the diet recovered undergrowth induced by FeCl3-injection into the cortex. Ordinate, average body weight; and abscissa, weeks after the injection. In each group, 13 (0–17 weeks) and seven rats (18–27 weeks) were used. Standard deviations at each point were within 7% of mean value. ○, HCl+CE group; □, HCl+EPC group; ●, Fe+CE group; and ■, Fe+EPC group.
Pathophysiology 2002 8, DOI: ( /S (02) )

9. Fig. 8
Effect of EPC-K1 on the development of seizure activity induced by FeCl3 in chronic experiments. Each rat was injected with 5 μl of FeCl3 solution (100 mM) into the motor cortex. The Fe+CE group was fed standard rat chow, and the Fe+EPC group was fed EPC-K1-supplemented diet. In ECoGs of No. 5–4 rat in the Fe+CE group, recurrent severe epileptiform activity was observed 1, 3 and 6 months after the injection. On the other hand, No. 4–3 rat in the Fe+EPC group showed no epileptiform activity until 6 months after the injection of FeCl3. The recordings were obtained by unipolar recording from the left occipital electrode. The position of the electrode and the drug injection site are shown in the lower right corner.
Pathophysiology 2002 8, DOI: ( /S (02) )

10. Fig. 9
Percent occurrence of epileptiform discharges in ECoG after FeCl3 injection into the rat motor cortex. Each rat was injected with 5 μl of FeCl3 solution (100 mM) into the motor cortex. The Fe+CE group was fed standard rat chow, and the Fe+EPC group was fed EPC-K1-supplemented diet. Percent occurrence of epileptiform discharges in the Fe+EPC group was significantly lower at 1 month and thereafter. ●, Fe+CE group; and ■, Fe+EPC group. Right-tilted harsh marks represent 95% confidence limit of percent occurrence of the Fe+CE group, and left-tilted show that of the Fe+EPC group. Number of total rats is in parentheses.
Pathophysiology 2002 8, DOI: ( /S (02) )

11. Fig. 10
Effect of EPC-K1 on the TBARS content in the focal area. Data express the TBARS content in the homotropic contralateral cortex as 100%. Relative TBARS content in the focal area significantly increased in the Fe+CE group rats 3 h, 3 and 7 days after the injection and in the Fe+EPC group rats 3 h after the injection, by the Mann–Whitney test. ○, HCl+CE group; □, HCl+EPC group; ●, Fe+CE group; and ■, Fe+EPC group. Mean±S.E.M. (N=5–6).
Pathophysiology 2002 8, DOI: ( /S (02) )

12. Fig. 11
Effect of EPC-K1 on the P-Carb content in the focal area. Data express the P-Carb content in the homotropic contralateral cortex as 100%. Relative P-Carb content in the focal area significantly increased in the Fe+CE and Fe+EPC group rats 3 h after the injection, by the Mann–Whitney test. ○, HCl+CE group; □, HCl+EPC group; ●, Fe+CE group; and ■, Fe+EPC group. Mean±S.E.M. (N=5–6).
Pathophysiology 2002 8, DOI: ( /S (02) )