Agric. Food Chem., 50:2488–2493, 2002.)
Srivastava, K.C., Effects of aqueous extracts of onion, garlic, and ginger on platelet aggregation and metabolism of arachidonic acid in the blood vascular system: in vitro study. Prostaglandins.
Leukotrienes Med., 13:227–235, 1984.
Xiao, H. and Parkin, K.L., Antioxidant function of selected allium thiosulfinate and S-alky(en)yl-L-cysteine sulfoxides, J. Agric. Food Chem., 50:2488–2493, 2002.
Allixin
Allixin (6-methyl-2-pentyl-4H-pyran-4-one) is one of the organosulfur compounds found in aged garlic extract. Kodera and
coworkers (1989) identified this phenolic compound in garlic that had weak antimicrobial activity. Subsequent research by Nishino et al. (1990) showed allixin was an anticancer agent by inhibiting skin cancer in mice induced by 7,12-dimethylbenz[α]-anthracene (DMBA) and the promoter, 12-O-tetradecanoyl (TPA).
Allixin. (From Moriguchi et al., Life Sci., 61:1413–1420, 1997. With permission.)
Allixin was also reported by Yamasaki et al. (1991) to inhibit aflatoxin B1-induced mutagenesis in Salmonella typhymurium, as well as the formation of aflatoxin B10DNA adducts. Moriguchi and coworkers (1997) examined the effect of allixin and its analogues on the survival and morphology of primary cultured neurons from fetal-rat brain. Allixin (1–100 ng/mL) significantly promoted the survival of neurons, as well as increased the number of branching points per axon in the hippocampal region. At higher concentrations (>1 microgram/mL), however, allixin was cy to toxic. Of the analogues examined, 2,6-dimethyl-3-hydroxy-4H-pyran-4-one (DHP) had potent neurotrophic activity at concentrations greater than 10 ng/mL without any cytotoxicity up to 10 microgram/mL.
DHP was considered to be a useful prototype as a prophylactic drug for the treatment of neurogenerative diseases. Allixin, a phytoalexin, is a stress compound produced by the plant when subjected to stress. Mahady and coworkers (2001) reported that allixin inhibited Helicobacter pylori. These researchers suggested reports that fresh garlic did not inhibit H.pylori growth were probably due to its absence of allixin, which is present only in stressed garlic.
References
Kodera, Y., Matsuura, H.m Susumu, Y., Toshihiko, S., Yoichi, I., Toru, F., and Hoyoku, N., Allixin, a stress compound from garlic, Chem. Pharm. Bull., 37:1656–1658, 1989.
Mahady, G.B., Allixin, a phytoalexin from garlic, inhibits the growth of Helicobacter pylori in vitro, Am. J. Gastroenterol., 96:3454–3455, 2001.
Moriguchi, T., Matsuura, H., Itakura, Y., Katsuki, H., Saito, H., and Nishiyama, N., Allixin, a phytoalexin produced by garlic, and its analogues as novel exogenous substances with neurotrophic activity, Life Sci., 61:1413–1420, 1997.
Nishino, H., Nishino, A., Takayasu, J., Iwashima, A., Itakura, Y., Kodera, Y., Matsuura, H., and Fuwa, T., Antitumor-promoting activity of allixin, a stress compound produced by garlic, Cancer J., 3:20–21, 1990.
Yamasaki, T., Teel, R.W., and Laum, B.H.S., Effect of allixin, a phytoalexin produced by garlic, on mutagenesid DNA-binding and metabolism of aflatoxin B1, Cancer Lett., 59:89–94, 1991.
S-Allyl-L-cysteine
S-Allyl-L-cysteine (SAC) is an organosulfur compound, which, together with allixin and its analogue, 2,6-dimethyl-3-hydroxy-4H-pyran-4-one (DHP), had antiaging,
S-Allyl-L-cysteine (SAC). (Adapted from Arnault et al., J. Pharm.
Biomed. Anal., 37:963–970, 2005.)
learning and memory improvement, neurotrophic effects, and antioxidant activity associated with aged garlic extract (Yamasaki et al., 1994; Moriguchi et al., 1996, 1997;
Nishiyama et al., 1997). Ito and coworkers (2003) showed SAC exerted a protective effect on amyloid β-protein-induced cell death in nerve growth, factor-differentiated PC 12 cells, a model of neuronal cells. Amyloid β-protein (Aβ), a 40–43 amino acid peptide, is involved with the formation of senile plaques in the brains of Alzheimer patients, as well as being cytotoxic to cultured neurons (Yao et al., 1999; Ekinci et al., 2000). SAC selectively protected neurons from Aβ-induced neurotoxicity. Kim and coworkers (2001) reported it was the antioxidant activity of garlic extract and SAC that differentially regulated nitric oxide in a murine macrophage by inhibiting iNOS expression and NF-κB activation while increasing nitric oxide in epithelial cells. This selectivity in regulation by garlic extract and SAC may contribute to their antiinflammatory effect and ability to prevent atherosclerosis.
The ability of SAC to prevent gentamicin renal damage was attributed by Maldonado et al. (2003) to its antioxidant properties. SAC reduced oxidative stress through preservation of Mn-SOD, glutathione peroxidase, and glutathione reductase activities.
References
Arnault, I., Haffner, T., Siess, M.H., Vollmar, A., Kahane, R., and Auger, J., Analytical method for appreciation of garlic therapeutic potential for validation of a new formulation, J. Pharm.
Biomed. Anal., 37:963–970, 2005.
Ekinci, F.J., Linsley, M.D., and Shea, T.B., Betaamyloid-induced calcium flux induces apoptosis in culture by oxidative stress rather than tau phosphorylation, Brain Res. Mol. Brain Res., 76:389–
395, 2000.
Ito, Y., Kosuge, Y., Sakikubo, T., Horie, K., Ishikawa, N., Obokata, N., Yokoyama, E., Yamashina, K., Yamamoto, M., Saito, H., Arakawa, M., and Ishige, K., Protective effect of S-ally-L-cysteine, a garlic compound, on amyloid β-protein-induced cell death in nerve growth factor-differentiated PC 12 cells, Neurosci. Res., 46:119–125, 2003.
Kim, K.-K., Chun, S.-B., Koo, M.-S., Choi, W.-J., Kim, T.-W., Kwon, Y.-G., Chung, H.-T., Billiar, T.R., and Kim, Y.-M., Differential regulation of NO availability from macrophages and endothelial cells by the garlic component, S-ally cysteine, Free Rad. Biol. Med., 30:747–756, 2001.
Maldonado, P.D., Barrera, D., Rivero, I., Mata, R., Medina-Campas, O.N., Hernandez-Pando, P., and Pedraza-Chaverri, J., Antioxidant S-ally lcy steine prevents gentamicin-induced oxidative stress and renal damage, Free Rad. Biol. Med., 35:317–324, 2003.
Moriguchi, T., Saito, H., and Nishiyama, N., Aged garlic extract prolongs longevity and improves spatial memory deficit in senescence accelerated mouse, Biol. Pharm. Bull., 17:395–307, 1996.
Moriguchi, T., Saito, H., and Nishiyama, N., Trophic effects of aged garlic extract (AGE) and its fractions on primary cultured hippocampal neurons from fetal rat brain, Phytother. Res., 10:472–486, 1997.
Nishiyama, N., Moriguchi, T., and Saito, H., Beneficial effects of aged garlic on learning and memory impairment in the senescence-accelerated mouse, Exp. Gerontol., 32:149–160, 1997.
Yamasaki, T., Li, L., and Lau, B.H., Garlic compounds protect vascular endothelial cells from hydrogen peroxide-induced oxidative injury, Phytother. Res., 8:408–412, 1994.
Yao, Z.X., Szweda, L.I., and Papadopoulus, V., Free radicals and lipid peroxidation do not mediate beta-amyloid-induced neuronal cell death, Brain Res., 847:203–210, 1999.
Almonds (Prunus amygdalus)
Almonds, popular tree nuts worldwide, are used in snack foods and as ingredients in bakery and confectionery products. Fraser (1999) pointed out that substituting almonds or walnuts for traditional fats in the human diet reduced LDL cholesterol by 8–12 percent.
Eating nuts is frequently associated with a substantial decrease in the risk of coronary heart disease of between 30–50 percent. In addition to their ability to reduce cholesterol, almonds have been reported to exhibit anticancer properties. Jenkins et al. (2002) compared whole almonds as a snack to low-saturated, whole-wheat muffins in a randomized, crossover study involving 27 men and women who consumed three isoenergetic supplements each for one month. The supplements contributed 22.2 percent of energy and were either fulldose almonds (73±3 g/d), half-dose of
TABLE A.2
Effect of Almonds on Blood Lipids of Hyperlipidemic Subjects1
Control Almonds
Half-dose Full-dose
Week 0 Treatment2 Week 0 Treatment2 Week 0 Treatment2
Cholesterol, mmol/L
Total 6.45
±0.1 6.44±0.1 5 6.47±0.1 6.25±0.15 6.60±0.1 6.21±0.15 LDL 4.34±0.1 4.22±0.1 3 4.30±0.1 4.10±0.12 4.45±0.1 4.01±0.12 HDL 1.43±0.0 1.14±0.08 1.38±0.0 1.43±0.08 1.40±0.0 1.45±0.09
Ratios
Total: HDL Choi. 4.95±0.2 4.89±0.24 5.07±0.2 4.68±0.24 5.00±0.2 4.58±0.23 LDL: HDL Choi. 3.32±0.0 3.23±0.18 3.40±0.2 3.11±0.20 3.40±0.1
8
dienes/LDL 14.8±0.6 14.3±0.5 15.3±0.8 13.4±0.6 14.1±0.6 12.9±0.03
1Values are mean±SEM. N=27.
2Treatment values represent the mean of weeks 2 and 4.
Source: Adapted from Jenkins et al., Circulation, 106:1327–1332, 2002.
almonds plus half-dose muffin, or a full-dose muffin. Significant changes in serum lipids were observed for almonds, which are summarized in Table A.2. Both half- and full-dose almonds significantly reduced LDL cholesterol and LDL: HDL cholesterol, while only full-dose almonds significantly affected lipoprotein and oxidized LDL levels. A linear response to almonds was observed, which suggested that for each 7-g portion of almonds, there was a 1 percent reduction in LDL cholesterol. It was apparent from this study, together with epidemiological data, that the consumption of almonds may reduce the risk of coronary heart disease.
Davis and Iwahashi (2001) showed wholealmond consumption significantly reduced aberrant crypt foci compared to wheat bran and cellulose, suggesting a possible reduction in colon-cancer risk. Takeoka and coworkers (2000) identified three triterpenoids in the hulls of almonds, including betulinic, oleanolic, and ursolic acids. Sang and coworkers (2001) isolated a new, prenylated benzoic acid, together with catechin, protocatechuic, and ursolic acids, in almond hulls. Many of these triterpenoids have been shown previously to have anti-inflamma tory, anti-HIV, and anticancer activities, suggesting almond hulls are rich sources of these bioactive compounds. Pinelo et al. (2004) recently showed almond-hull extracts had almost 60 percent higher antioxidant capacity compared to pine sawdust, in spite of being much lower in phenolic compounds.
References
Davis, P.A. and Iwahashi, C.K., Whole almonds and almond fractions reduce aberrant crypt foci in a rat model of colon carcinogenesis, Cancer Lett., 165: 27–33, 2001.
Fraser, G.E., Nut consumption, lipids, and risk of a coronary event, Clin. Cardiol., 22(Suppl. 7):III, 11–5, 1999.
Jenkins, D.J.A., Kendall, C., Marchie, A., Parker, T., Connelly, P.W., Quian, W., Haight, J., Faulkner, D., Vidgen, E., Lapsley, K.G., and Spiller, G.A., Dose response of almonds on coronary heart disease risk factors: Blood lipids, oxidized low-density lipoproteins, lipoprotein (a), homocysteine, and pulmonary nitric oxide: A randomized, controlled, crossover trial, Circulation, 106:1327–1332, 2002.
Pinelo, M., Rubilar, M., Siniero, J., and Nunez, M.J., Extraction of antioxidant phenolics from almond hulls (Prunus amygdalus) and pine sawdust (Pinus piaaster), Food Chem., 85:267–273, 2004.
Sang, S., Lapsley, K., Rosen, R.T., and Ho, C.-T., New prenylated benzoic acid and other
constituents from almond hulls (Prunus amygdalus Batsch), J. Agric. Food Chem., 50:607–609, 2001.
Takeoka, G., Dao, L., Teranishi, R., Wong, R., Flessa, S., Harden, L., and Edwards, R.,
Identification of three terpenoids in almond hulls, J. Agric. Food Chem., 48:3437–3439, 2000.