Hepatoprotection by chemical constituents of the marine brown alga Spatoglossum variabile: A relation to free radical scavenging potential

Figures & data

Table 1.  In vitro radical scavenging activities.

Compound	IC50 (µM)^a
	DPPH	NADH/PMS	XO^b
1	72 ± 1.20	—	>1000
2	138 ± 0.54	—	>1000
3	54 ± 0.05	95 ± 1.77	>1000
4	92 ± 1.00	87 ± 1.08	>1000
Propyl gallate^c	30 ± 0.25	106 ± 1.7	628 ± 5.0
Allopurinol^d	—	—	7. 5 ± 0.17

—, inactive; DPPH, 1,1-diphenyl-2-picrylhydrazyl radicals; NADH, β-nicotinamide adenine dinucleotide; PMS, 5-methylphenazium methyl sulfate.

^aIC₅₀ values are the mean ± SEM of five assays. ^bXanthine oxidase. ^cStandard antioxidant. ^dStandard inhibitor of XO.

Figure 1  . Cinnamic acid ester and aurone derivatives from Spatoglossum variabile: (1) n-Butyl 3,5-dimethoxy-4-hydroxycinnamate; (2) isopropyl 3,5-dimethoxy-4-hydroxycinnamate; (3) 4′-chloro-2-hydroxyaurone; (4) 4′-chloroaurone.

Figure 2  . Proposed mechanism of removal of hydrogen atom from aurone derivative.

Table 2.  Effects of pretreatment with chemical constituents of marine brown alga Spatoglossum variabile on serum AST and ALT and bilirubin in CCl₄-intoxicated Wistar rats (n = 6).

Groups	sAST^a (IU/mL)	sALT^a (IU/mL)	Bilirubin (mg %)^a
			Total	Direct	Indirect
Normal control^b	157.5 ± 13.2	71.8 ± 3.04	0.126 ± 0.060	0.023 ± 0.015	0.103 ± 0.066
Pathological control^c	1715.5 ± 144.5	1557 ± 48.7	0.824 ± 0.081	0.254 ± 0.031	0.576 ± 0.089
CCl4+ compound 1	1564.0 ± 235.8	869.8 ± 194.5*	0.338 ± 0.085*	0.070 ± 0.004*	0.268 ± 0.086*
CCl4+ compound 2	196.3 ± 5.49*	83.7 ± 9.48*	0.048 ± 0.010*	0.018 ± 0.004*	0.030 ± 0.009*
CCl4+ compound 3	199.3 ± 12.2*	89.0 ± 15.73*	0.085 ± 0.005*	0.033 ± 0.004*	0.053 ± 0.005*
CCl4+ compound 4	214.3 ± 10.7*	149.5 ± 16.5*	0.093 ± 0.004*	0.020 ± 0.004*	0.073 ± 0.002*
Propyl gallate^d	559.0 ± 84.7*	607.5 ± 127.9*	0.318 ± 0.056*	0.145 ± 0.012*	0.173 ± 0.030*

sAST, serum aspartate aminotransferase, sALT, serum alanine aminotransferase.

^aValues of sAST, sALT, and bilirubin are the mean ± SEM of six Wistar rats. ^bVehicle control and received only normal saline. ^cPathological control group received i.p. dose of 20% CCl₄ diluted with edible oil (1 mL/100 g body weight). ^dStandard antioxidant.

*Statistically significant differences were defined as values less than p < 0.05. Results were evaluated by performing analysis of variance (ANOVA).

Table 3.  In vitro β-glucuronidase inhibitory activities.

Compound	IC50 (µM)^a	Ki (µM)^b	Type of inhibition
1	23.4 ± 3.0	28.0 ± 1.23	Mixed-type
2	276.2 ± 10.0	680 ± 3.0	UC^c
3	—	—	—
4	1000 ± 30.0	×	×
Saccharic acid 1, 4-lactone^d	0.8 ± 0.002	0.17^e	Competitive^e

—, inactive; ×, not done.

^aIC₅₀ values are the SEM of five values. ^bK_i is the mean of three values calculated using Dixon plot and Lineweaver Burk secondary plots. ^cUncompetitive inhibitor. ^dStandard inhibitor. ^eFrom earlier reports (Schomberg & Salzmann, 1991).

Figure 3  . Steady-state inhibition of β-glucuronidase by n-butyl 3,5-dimethoxy 4-hydroxyl cinnamate 1: (A) Lineweaver-Burk plot of reciprocal of the initial velocities versus reciprocal of p-nitrophenyl-β-d-glucuronide concentrations. (B) Dixon plot of reciprocal of the initial velocities versus various concentrations of inhibitor. Each point in the graphs represents the mean of three experiments.

Figure 4  . Steady-state inhibition of β-glucuronidase isopropyl 3,5-dimethoxy 4-hydroxyl cinnamate 2: (A) Lineweaver-Burk plot of reciprocal of the initial velocities versus reciprocal of p-nitrophenyl-β-d-glucuronide concentrations. (B) Dixon plot of reciprocal of the initial velocities versus various concentrations of inhibitor. Each point in the graphs represents the mean of three experiments.

Table 4.  Cytotoxicity against human neutrophils.

Compound	ED50 (µg/mL)^a
1	63.24 ± 2.63
2	148.56 ± 1.02
3	200 ± 4.40
4	>200

^aED₅₀ values are the mean ± SEM of five assays.

Schomberg D, Salzmann M. (1991). Enzyme Handbook. Berlin/New York: Springer-Verlang.

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