Table 1: Total cholesterol level

Groups	12h	24h	72h	120h
NCG	149.49±6.598	148.96±8.601	146.74±9.790	149.91±5.560
HCG	311.66±2.70	385.06±3.98	271.47±4.98	225.89±7.86
HG	326.61±3.87	376.22±9.59	263.76±3.061	217.1±9.902
HGCaM	222.52±5.68**	205.53±2.80**	189.08±5.541**	163.01±4.581**
HGCaAS	183.19±6.43**	171.8±2.964**	169.51±4.048**	158.39±7.417**
HGCaAIS	167.92±4.65**	165.48±2.61**	161.82±2.613**	151.315±5.324**

Values are means ± SEM from five animals in each group. NCG: normal control group; HCG: hyperlipidemic control group; HG: hyperlipidemic+2% PVP; HGCaM: total methanolic extract treated group; HGCaAS: aqueous fraction treated group; HGCaAIS: aqueous insoluble treated group HCG and HG are compared with NCG. HGCaM, HGCaAS, and HGCaAIS are compared with HCG, **P < 0.01.

Table 2: Total Triglycerides Level

Groups	12h	72024h	72h	120h
NCG	72.63±8.31385	69.73±5.310	71.03±4.345	70.08±6.282
HCG	233.18±5.930	298.69±7.341	118.01±14.64	96.98±5.980
HG	242.87±9.870	269.59±8.897	106.07±7.980	81.97±9.89
HGCaM	96.286±12.76**	90.22±15.720**	65.04±14.932**	69.41±12.98^NS
HGCaAS	71.28±18.980**	81.80±12.760**	60.60±10.54**	76.09±8.876^NS
HGCaAIS	53.67±10.896**	59.85±19.865**	64.25±12.89**	71.67±7.670**

Table 3: HDL-C Level

Groups	12h	24h	72h	120h
NCG	98.89±3.57	92.87±6.854	95.86±3.65	99.35±9.45
HCG	106.95±12.870	119.63±2.140	110.76±7.640	97.85±1.650
HG	112.84±9.430	115.64±2.76	106.65±4.87	90.96±3.590
HGCaM	115.8874±13.549^NS	99.56±9.132^NS	98.60±6.670^NS	87.64±2.480^NS
HGCaAS	120.66±8.443^NS	107.88±6.560^NS	112.82±5.880^NS	108.76±1.990^NS
HGCaAIS	136.32±3.570^NS	166.73±2.430^NS	138.43±2.654^NS	110.83±3.880^NS

Table 4: LDL-C Level

Groups	12h	24h	72h	120h
NCG	36.085±1.27	42.16±3.69	36.67±5.32	27.2±5.5
HCG	157.09±10.240	205.7±4.30	137.11±5.60	109.86±5.20
HG	166.55±7.50	207.78±5.70	135.87±3.30	108.76±4.330
HGCaM	87.53±5.70**	87.93±9.40**	72.47±4.10**	62.48±3.41**
HGCaAS	48.25±5.84**	47.57±6.30**	44.65±3.90**	35.43±3.51**
HGCaAIS	20.87±4.14**	13.22±3.70**	10.65±2.50**	25.97±1.980**

Table 5: Atherosclerosis Index

Groups	12h	24h	72h	120h
NCG	0.48±0.142	0.60±0.26	0.53±0.38	0.50±0.21
HCG	1.91±0.28	2.2±0.11	1.45±0.20	1.30±0.02
HG	1.89±0.19	2.25±0.21	1.47±0.22	1.38±0.10
HGCaM	0.92±0.18*	1.06±0.20*	0.91±0.15^NS	0.86±0.02^NS
HGCaAS	0.51±0.14**	0.59±0.11**	0.50±0.12^NS	0.45±0.01^NS
HGCaAIS	0.28±0.10**	0.007±0.01**	0.16±0.12**	0.36±0.02^*

Table 6: LDL-C/HDL-C

Groups	12h	24h	72h	120h
NCG	0.36±0.10	0.45±0.05	0.38±0.01	0.29±0.06
HCG	1.46±0.011	1.71±0.01	1.23±0.04	1.12±0.05
HG	1.47±0.021	1.79±0.02	1.27±0.02	1.19±0.02
HGCaM	0.75±0.06**	0.88±0.011**	0.73±0.01**	0.71±0.02**
HGCaAS	0.39±0.01**	0.44±0.03**	0.39±0.02**	0.32±0.01**
HGCaAIS	0.15±0.03**	0.079±0.02**	0.076±0.01**	0.23±0.032 **

2.4 Experimental animal protocol:

Overnight fast rats were divided into six groups of five rats each. The first group served as normal control (NCG), received intraperitoneal administration of normal saline and water by gavage; the second hyperlipidaemic control group (HCG), was treated with intraperitoneal injection of Triton WR-1339 (Tyloxapol,Sigma–Aldrich, USA) at a dose of 400 mg/kg in normal saline and gavaged with distilled water; third hyperlipidaemic group (HG), was treated with intraperitoneal injection of Triton WR-1339 (Tyloxapol,Sigma–Aldrich, USA) at a dose of 400 mg/kg in normal saline and gavaged with PVP 2% v/v , in the fourth group (HG + CaM), the animals were also treated with intraperitoneal injection of Triton (400 mg/kg BW) followed by intragastric administration of Chenopodium album Methanolic extract (400mg/kg); the fifth group (HG + CaAS) received intraperitoneal injection of Triton (400 mg/kg) followed by an intragastric administration of crude aqueous extract (100mg /kg BW); dissolved in PVP water mixture (2% v/v). The last group (HG+CaAIS) received intraperitoneal injection of Triton (400 mg/kg) followed by an intragastric administration of crude aqueous insoluble extract (100mg/kg) dissolved in PVP water mixture (2% v/v). The treatment was continued for 5 days and the blood samples were taken after 12h, 24h, 72h and 120h with a view to see the effect of drug on lipid profile. The blood samples were withdrawn from the eye vein and transferred directly into centrifuge tubes and allowed to clot at room temperature for 20–25 min and centrifuged for 15–20 min at 2000 r.p.m. The supernatant clear serum thus obtained was transferred carefully with the help of micropipette into small test tubes for estimation.

2.5 Biochemical analysis of plasma:

The plasma total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol were quantified using enzymatic kits (Sigma Diagnostic, Inc., USA). The LDL-cholesterol was calculated by the Friedwald formula: ^[5]

LDL-Cholesterol = Total cholesterol - [HDL-Cholesterol + (Triglyceride/5)]

2.6 Atherogenic index (AI):

The AI and was calculated by the following formula: AI = (total cholesterol -HDL-C) /HDL-C and LDL-C/HDL-C ratio was calculated as the ratio of plasma LDL-C to HDL-C levels.

2.7 Statistical analysis:

Data obtained were analyzed using the Student’s t-test and a P values less than 0.05 was considered statistically significant. Our results were expressed as means ± SEM.

3. RESULTS:

3.1 Induction of hyperlipidaemia with Triton WR-1339:

The levels of plasma cholesterol and triglyceride in NCG, HCG, HG, HGCaM, HGCaAS and HGCaAIS after 12h, 24 h, 72h and 120h from treatments are reported in Tables 1 and 2 respectively. In comparison with NCG, Triton WR-1339 caused a marked increase in cholesterol and triglyceride plasma concentrations measured after 12 or 24 h but have shown a decrease in cholesterol and triglyceride plasma concentration after 72 and 120hr injection. After 12 h and 24h the plasma total cholesterol was increased by 52.03% and 61.31% in HCG and by 54.22% and 60.40% in HG while triglycerides was increased by 68.95% and 76.65% in HCG and by 76.65% and 74.13% in HG, respectively but at 72 and 120h the effect of triton was only 45-30% for total cholesterol and triglycerides level for both HCG and HG group. HDL and LDL-cholesterol levels in NCG, HCG, HG, HGCaM, HGCaAS and HGCaAIS after 12h, 24 h, 72h and 120h from treatments are reported in Tables 3 and Table 4. Neither at 12 h nor at 24 h was the HDL cholesterol significantly changed in both HCG and HDCG with respect to their relative control group (NCG), while a significant increase on LDL-cholesterol levels occurred at 12h and 24h and was maintained until 120h from Triton injection. LDL-cholesterol concentrations in HCG and HDCG were respectively, 77.03% and 78.33% after 12h and by 79% after 24h higher than those in normal control grouped. Also the increase of this parameter was partially reduced to 7-8% in HCG and HDCG after 72h and 120h.

Table 5 and 6 shows the changes of atherogenic index (AI) and LDL-C/HDL-C ratio in control and treated mice. It appears clear from these results that the Triton administration significantly affects the cardiovascular risk markers. Indeed, the AI was statistically increased in both HCG and HDCG by 73% when compared with values found in their relative normolipidemic control at 12h and 24h while the values were partially reduced to 13% after 72h and 120h.Besides, there were significant further increases of LDL-C/HDL-C ratios in Triton-injected animals (HCG and HDCG). In contrast to normolipidemic mice, after 12h and 24h Triton treatment produced an elevated ratio either in hyperlipidemic group animals 74-75% in HCG and HG when compared to NCG, This changing pattern was maintained until 120h.

3.2 Effect of Chenopodium album extracts on mice plasma lipid profile:

3.2.1 Total cholesterol and Plama triglycerides:

The plasma total cholesterol and triglyceride levels of its methanolic extract and its fractions-treated mice are shown in Tables 1 and 2. Notably, the eminent total cholesterol concentrations produced by Triton administration after 12h and 24h were significantly (P values <0.01) suppressed by more than 25-40% in animals gavaged with crude methanolic extract (HGCaM).However, the reduction of total cholesterol by aqueous insoluble extract (HGCaAIS) extract was marked (46.12% to 57.02% P < 0.01) after 12h and 24h of triton administration while effect was only (40.39 to 33.01% p<0.01) after 72h and 120h. Total cholesterol was suppressed by (41.55% to 55.38% p<0.01) after 12h and 24h and by (37.55% and 29.88% p<0.01) after 72h and 120h compared to its relative hyperlipidemic control group (HDCG) in the aqueous soluble extract.

Although the plasma TG levels of the mice treated with crude methanolic extract were suppressed by (58.70% and 69.79% p<0.01) at 12h and 24h but at 120h plasma triglycerides were not significantly decreased (28.42% p>0.05) with respect to the level found in animals of HGCG. Aqueous insoluble fractions were significantly decreased to (76.98% and 79.96% p<0.01) at 12h and 24h and (48.64% and 21.54% p<0.01) at 72h and 120h. Water soluble fraction were statistically decreased (69.43 and 72.61% p<0.01) at 12h and 24h but the results were not significantly deceased (21.54% p>0.05NS) with respect to the levels found in animals of HDCG.

3.2.2 HDL and LDL-cholesterol:

Differences in blood HDL-C by (11.36% and 29.37%) between aqueous soluble (HGCaAS) and aqueous insoluble (HGCaAIS) extracts groups were observed after 12h of triton treatment. In disparity, 24 h after treatment, both aqueous soluble and aqueous insoluble fractions substantially increase of HDL-C levels, by 10.89 and 28.24%, respectively (Table 3). The levels of this cholesterol fraction also tended to increased but the changing pattern remained statistically insignificant. All other plant extracts showed a significant ameliorative action on plasma elevated LDL-cholesterol caused by TritonWR-1339 .Certainly, 12 h after the beginning of the experiment, the significant (P < 0.01) decreases of plasma LDL-C were 44.40%, 69.28% and 86.71% in HGCaM, HGCaAS and HGCaAIS respectively and after 24h a significant decrease of plasma LDL-C was 57.25%, 76.87% and 70.44% in HGCaM, HGCaAS and HGCaAIS respectively. But at the end of the experiment (120 h), the elevated values of LDL-C were 43.12%, 67.74% and 76.36% in HGCaM, HGCaAS and HGCaAIS respectively at significance levels similar to that obtained at 12 h, 24h and 72h compared to the HCG (Table 4).

3.2.3. Atherogenic index (AI) and LDL-C/HDL-C ratio:

AI lowered by the methanolic extract, aqueous soluble and aqueous insoluble extract of Chenopodium album in Triton-induced hyperlipidemic mice were found as reported in Table5. Though, all extracts showed an improvement of the cardiovascular risk level by the decrease of AI in the treated groups (HGCaM, HGCaAS and HGCaAIS) by (51.83% and 51.81% p<0.05) at 12h and 24 hr while no significant differences in AI between any treated groups (65.31% and 65.38% p>0.05 NS) were observed at 72h and 120h. Aqueous soluble fractions has shown statistically significant lower in AI (73% p<0.01) at 12h and 24h and the results were non significant after 72h and 120h (65% p>0.05 NS). In contrast elevated AI were statistically decreased (85.34%, 99.68% and 88%) after 12h, 24h and 72h and it become significant (72.30% p<0.05) after 120h of triton administration.

The ratio of LDL-C to HDL-C is also a predictive indicator of cardiovascular disease incidence. The Triton injection produced a significant increase of this marker. All the extract has statistically change it ( p<0.01), either at 12 h, 24 h, 72h and 120h after treatment (Table 6).

4 DISCUSSIONS AND CONCLUSION:

The non-ionic detergent, Triton WR-1339, has been widely used to block the uptake of triacyl glycerol-rich lipoproteins from the circulation by extra hepatic tissues resulting in an increase in the level of circulatory lipoprotein in order to produce acute hyperlipidemia in animal models which are often used for a number of objectives, in particular for screening natural or chemical hypolipidemic drugs. ^[6] With this aim, many medicinal plants, such as Phylanthus nuriri, have been assessed for their hypolipidemic activity in a Triton WR-1339-induced hyperlipidemic model. ^[7] In fact, Schurr demonstrated that parenteral administration of Triton induced hyperlipidemia in adult rats; maximum blood cholesterol and triglyceride levels were reached at 20 h, followed by a decline to normal values. Similar results were reported while investigating with the hypolipidemic activity of Muccuna pruriens.^[8] In our hands, this model gave similar plasma lipid profile elevated changes, both at 12 h and at 24h after and a decline to normal value after Triton WR-1339 injection in mice. This result demonstrates the feasibility of using Triton induced hyperlipidemic mice as an experimental model to investigate the hypolipidemic effect of Chenopodium album extracts.This work was aimed at the assessment of the possible hypocholesterolemic and hypotriglyceridemic activities of methanolic with its aqueous soluble and aqueous insoluble Chenopodium album extracts. And it is clear our results that the methanolic extract with its aqueous and aqueous insoluble fraction from this plant C. album decrease plasma total cholesterol in a marked manner, 12 h, 24 h, 72h and 120h after Triton treatment. The large increase in plasma cholesterol and triglycerides due to Triton WR-1339 injection results mostly from an increase of VLDL secretion by the liver accompanied by a strong reduction of VLDL and LDL catabolism.^[9]Thus, since the proportion of triglyceride in VLDL is several times higher than cholesterol, it is not surprising that the hypolipidaemic action of Chenopodium album extract was markedly higher for triglycerides than for cholesterol. This result suggests that the extract is able to restore, at least partially, catabolism of lipoproteins. The underlying mechanisms of this activity is not elucidated by present study, however, as hypothesised by many works with other plants the restoration of catabolic metabolism of VLDL could be due to an increased stimulation of the lipolytic activity of plasma lipoprotein lipase with a decrease of its LDL fraction which is a major, potentially modifiable risk factor of cardiovascular diseases and the target of many hypocholesterolemic therapies. ^{[10, 11]} This result also suggests that cholesterol-lowering activity of the herb extract can be result from the rapid catabolism of LDL cholesterol through its hepatic receptors for final elimination in the form of bile acids as demonstrated by many workers when studying the lipid lowering activity of Phyllantus niruri in hyperlipemic rats.^[12] However, this hypothesis needs to be validating by an experimental study. In addition, the aqueous soluble and aqueous insoluble fractions showed protective action by the increase of HDL-cholesterol levels, which is reported to have a preventive function against atherogenesis. Since an independent inverse relationship between blood HDL-C levels and cardiovascular risk incidence has been documented and reported beyond any doubt. ^[13]This lipoprotein called ‘‘good cholesterol” facilitates the mobilisation of triglycerides and cholesterol from plasma to liver where it is catabolised and eliminated in the form of bile acids. The possible mechanism of this activity may result from the enhancement of lecithin cholesteryl. Acyl transferase (LCAT) and inhibition of hepatic triglyceride lipase (HTL) on HDL which may lead to a rapid catabolism of blood lipids through extrahepatic tissues.^[14] It is also recently reported that triglycerides play a key role in the regulation of lipoprotein interactions to maintain normal lipid metabolism. Indeed, the elevated plasma TGs levels were associated with an increased incidence of coronary artery disease. ^[15]Moreover, these higher plasma TG levels have been attributed mainly to an increased population of small, dense LDL deposits which are very atherogenic and enhanced cholesteryl ester mass transfer from apolipoprotein B-containing lipoproteins (VLDL and LDL). ^[16] TGs have also been proposed to be a major determinant of cholesterol esterification, its transfer and HDL remodeling in human plasma. ^[17] Both aqueous soluble and aqueous insoluble methanolic fractions from C. album significantly suppressed the elevated blood concentrations of TGs. This decreasing effect of the extract and its fractions is very spectacular especially by both stimulation of the gene expression of lipoprotein lipase leading to enhanced catabolism of VLDL, synthesis of fatty acids and reduced VLDL secretion. This result suggests that the extracts are able to restore, at least partially, the catabolism of triglycerides. The underlying mechanism of this activity is not elucidated by the present study. However, as hypothesised by many works with other plants, ^[18-20] the restoration of catabolic metabolism of triglycerides could be due to an increased stimulation of the lipolytic activity of plasma lipoprotein lipase (LPL).Administration of Chenopodium album extract provides a beneficial action on mice lipid metabolism in regard to the reduction of AI. In fact, the AI was deceased in all fractions treated groups. Similar results were reported by others when studying the hypolipidemic effect of natural products. ^[21] This ameliorative action was due to the plasma lipid-lowering activity of different fractions.It is also desirable to have higher plasma HDL and lower LDL-cholesterol to prevent atherogenesis, since there is a positive correlation between an increased LDL-C/HDL-C ratio and the development of atherosclerosis. Again, the administration of Chenopodium album extracts and its fractions significantly suppressed the higher values of LDL-C/HDL-C ratio showing the beneficial effect of this plant in preventing atherosclerosis incidence. The results found clearly demonstrate that the bioactive compound(s) contained in this plant have a polar character since they are more soluble in water and polar organic solvents. This finding is in agreement with previous reports showing that plant methanol, water soluble and water insoluble extracts possess cholesterol-suppressive capacities and an ability to attenuate the accelerated development of atherosclerosis in hypercholesterolemic models.In fact, flavonoids and tannins, a heterogeneous group of ubiquitous plant polyphenols, exhibit different pharmacological activities, including hypolipidemic and anti-atherogenic effects.^{[22, 23]}Thus through its preliminary phytochemical screening we can suggest that flavonoids and tannins are the major compounds responsible for the hypolipidemic activity of chenopodium album extract. Furthermore, qualitification of total phenol, tannin, and flavonoid contents in plant samples by prelimary phytochemical screening confirmed the results reported by demonstrating that these aqueous soluble and aqueous insoluble fractions represent major polar compounds of Chenopodium album. Again, the finding strongly suggests that the hypolipidaemic activity of this plant could be attributed to the presence of valuable polyphenolic compounds. ^[24]This result is considered important for the treatment of hyperlipidemia-induced atherosclerosis and apparently validates the folk medicinal use of Chenopodium album linn by hyperlipidemic patients in east of India. Therefore, further studies are necessary to elucidate the exact mechanisms of the Chenopodium album Linn effect on plasma lipid parameters, including the activity of purified compounds and dose response effects.

REFERENCES:

1. Wald NJ and Law MR. Serum cholesterol and ischaemic heart disease. Atherosclerosis. 1995; 118 (Suppl): S1−S5.

2. Rader DJ. A new feature on the cholesterol-lowering landscape. Natural Medicines. 2001; 7(12): 1282−1284.

3. Clapham AR, Tutin TG, and Warburg EF. 1962. Flora of the British Isles. Cambridge University Press. 1962; 7

4. Siddiqui I. and Bajwa R. Variation in weed composition in wheat fields of Lahore and Gujranwala divisions. Pak. J. Biol. Sci 2001; 4 (Supplement): 492-504.

5. Friedman M, Bayer SO, The Mechanism underlying hypocholesterolemia induced by Triton WR 1339. American journal of Physiology. 1957; 190: 439-445.

6. Schurr PE, Schultz JR., and Parkinson, T. M. Triton induced hyperlipidaemia in rats as an animal model for screening hypolipideamic drugs. Lipids. 1972; 7:69–74.

7. Khanna AK, Rizvi F, and Chander R. Lipid lowering activity of Phyllanthus niruri in hyperlipemic rats. Journal of Ethnopharmacology. 2002; 82: 19–22

8. Lauk L, Galati EM, Forestieri AM, Kirjavainen S, and Trovato A. Mucuma pruriens infusion lowers cholesterol and total lipid plasma levels in the rats. Phytotherapy Research. 1989; 3(6) 263–264.

9. Otway S , Robinson D S , The effect of the nonionic detergent (Triton) on the removal of triglyceride fatty acids from the blood of the rats. Journal of Physiology. 1967; 190, 309–319.

10. Campillo JE, Torres MD, Dominguez E, Romero A, P´erez C, Ficus carica leaf administration reduces hypertriglyceridaemia in streptozocin diabetic rats. Diabetologia. 1994; 37: 213.

11. Pe´rez C, Canal JR, Campello JE, Adelaida R, and Torres, MD. Hypotriglyceridaemic Activity of Ficus carica Leaves in Experimental Hypertriglyceridaemic Rats. Phytotherapy Research.1999; 13: 188–191.

12. Khanna AK, Rizvi F, and Chander R. Lipid lowering activity of Phyllanthus niruri in hyperlipemic rats. Journal of Ethnopharmacology 2002; 82: 19–22

13. Malloy MJ and Kan JP. Medical management of hyperlipidemic states. Advances in Internal Medicine. 1994; 39: 603–631.

14. Anila L, and Vijayalakshmi NR. Flavonoids from Emblica officinalis and Mangifera indica-effectiveness for dyslipidemia. Journal of Ethnopharmacology. 2002; 79: 81–87.

15. Hokanson JE, and Austin MA. Plasma triglyceride level is a risk factor to cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population based prospective studies. Journal of Cardiovascular Risk. 1996; 3: 213–219.

16. Gue´rin M, Le Goff, W, Lassel TS, Van TA, Steiner, G, and Chapman MJ. Proatherogenic role of elevated CE transfer from HDL to VLDL1 and dense LDL in type 2 diabetes. Arteriosclerosis Thrombosis and Vascular Biology. 2001; 21: 282–289.

17. Murakami T, Michelagnoli S, Longhi R, Gianfranceschini G, Pazzucconi F, Calabresi L, et al. Triglycerides are major determinants of cholesterol esterification/transfer and HDL remodeling in human plasma. Arteriosclerosis Thrombosis and Vascular Biology. 1995; 15: 1819–1828.

18. Pe´rez C, Canal JR, Campello JE, Adelaida R, and Torres MD. Hypotriglyceridaemic Activity of Ficus carica Leaves in Experimental Hypertriglyceridaemic Rats. Phytotherapy Research. 1999; 13: 188–191.

19. Sudheesh S, Presannakumar G, Vijayakumar S, and Vijayalakshmi NR. Hypolipidemic effect of flavonoids from Solanum melongena. Plant Foods for Human Nutrition. 1997; 51: 321–330.

20. Xie W, Wang W, Su H, Xing D, Cai G, and Du L. Hypolipidemic Mechanisms of Ananas comosus L. Leaves in Mice: Different from Fibrates but Similar to Statins. Journal of Pharmacological Sciences. 2007; 103: 267–274.

21. Cherng J Y and Shih MF. Preventing dyslipidemia by Chlorella pyrenoidosa in rats and hamsters after chronic high fat diet treatment. Life Sciences. 2005; 76: 3001–3013.

22. Del Bas JM, Ferna´ndez-Larrea J, Blay M, Arde`vol A, Salvado MJ, Arola, L, et al. Grape seed procyanidins improve atherosclerotic risk index and induce liver CYP7A1 and SHP expression in healthy rats. FASEB Journal. 2005; 19: 479–481.

23. Lee JH, Seo WD, Jeong SH, Jeong TS, Lee WS, and Park KH. Human Acyl-CoA: Cholesterol Acyltransferase Inhibitory Effect of Flavonoids from Roots of Glycine max (L.) Merr. Agricultural Chemical and Biotechnology. 2006; 49:57–61.

24. Javanmardia JB, Stushnoffb,C, Lockeb E, and Vivancob JM. Antioxidant activity and total phenolic content of Iranian Ocimum accessions. Food Chemistry. 2003; 83: 547–550.

Received on 27.08.2009 Modified on 23.10.2009

Research J. Pharm. and Tech. 3(1): Jan.-Mar. 2010; Page 187-192