Antioxidant activity of selected Indian spices

Spices and vegetables possess antioxidant activity that can be applied for preservation of lipids and reduce lipid peroxidation in biological systems. The potential antioxidant activities of selected spices extracts (water and alcohol 1:1) were investigated on enzymatic lipid peroxidation. Water and alcoholic extract (1:1) of commonly used spices (garlic, ginger, onion, mint, cloves, cinnamon and pepper) dose-dependently inhibited oxidation of fatty acid, linoleic acid in presence of soybean lipoxygenase. Among the spices tested, cloves exhibited highest while onion showed least antioxidant activity. The relative antioxidant activities decreased in the order of cloves, cinnamon, pepper, ginger, garlic, mint and onion. Spice mix namely ginger, onion and garlic; onion and ginger; ginger and garlic showed cumulative inhibition of lipid peroxidation thus exhibiting their synergistic antioxidant activity. The antioxidant activity of spice extracts were retained even after boiling for 30 min at 100 degrees C, indicating that the spice constituents were resistant to thermal denaturation. The antioxidant activity of these dietary spices suggest that in addition to imparting flavor to the food, they possess potential health benefits by inhibiting the lipid peroxidation.     

十八种辛香料对五种食源性致病菌的抑菌研究(英文)

本实验研究18种辛香料对五种食源性病原菌:单增李斯特菌,大肠杆菌O157∶H7,肠炎沙门氏菌,副溶血性弧菌和金黄色葡萄球菌的抑制作用。辛香料以60℃蒸馏水浸提。研究各种辛香料的最低抑菌浓度(80~5 mg/mL)以及经100℃处理15 m in和121℃处理15 m in的稳定性。结果表明,大部分辛香料具有良好的抑菌效果,尤其是丁香和桂皮对副溶血弧菌和金黄色葡萄球菌的最低抑菌浓度为5 mg/mL。经热处理部分香料失去了抑制作用,如八角,茴香,五香粉,海南白和黑胡椒,但大多数香料保持抑菌效果。这些结果表明,香料可抑制感染海产品的病原菌,同时在加工香料的过程中应该避免高温处理。     

Spice phenolics inhibit human PMNL 5-lipoxygenase

A wide variety of phenolic compounds and flavonoids present in spices possess potent antioxidant, antimutagenic and anticarcinogenic activities. We examined whether 5-lipoxygenase (5-LO), the key enzyme involved in biosynthesis of leukotrienes is a possible target for the spices. Effect of aqueous extracts of turmeric, cloves, pepper, chili, cinnamon, onion and also their respective active principles viz., curcumin, eugenol, piperine, capsaicin, cinnamaldehyde, quercetin, and allyl sulfide were tested on human PMNL 5-LO activity by spectrophotomeric and HPLC methods. The formation of 5-LO product 5-HETE was significantly inhibited in a concentration-dependent manner with IC(50) values of 0.122-1.44 mg for aqueous extracts of spices and 25-83 microM for active principles, respectively. The order of inhibitory activity was of quercetin>eugenol>curcumin>cinnamaldehyde>piperine>capsaicin>allyl sulfide. Quercetin, eugenol and curcumin with one or more phenolic ring and methoxy groups in their structure showed high inhibitory effect, while the non-phenolic spice principle allyl sulfide showed least inhibitory effect on 5-LO. The inhibitory effect of quercetin, curcumin and eugenol was similar to that of synthetic 5-LO inhibitors-phenidone and NDGA. Moreover, the inhibitory potency of aqueous extracts of spice correlated with the active principles of their respective spices. The synergistic or antagonistic effect of mixtures of spice active principles and spice extracts were investigated and all the combinations of spice active principles/extracts exerted synergistic effect in inhibiting 5-LO activity. These findings clearly suggest that phenolic compounds present in spices might have physiological role in modulating 5-LO pathway.     

Are summit metabolism and thermogenic endurance correlated in winter-acclimatized passerine birds?

Small birds exhibiting marked winter improvement of cold tolerance also show elevated summit metabolic rates (maximum cold-induced metabolic rate) in winter relative to summer. However, relatively large increases in cold tolerance can occur with only minor increments of maximum cold-induced metabolic rate and geographic variation in cold tolerance is not always positively correlated with variation in maximum cold-induced metabolic rate. Thus, it is uncertain whether maximum cold-induced metabolic rate and cold tolerance are phenotypically correlated in small birds and no previous study has directly examined this relationship. I measured maximum cold-induced metabolic rate and cold tolerance (i.e., thermogenic endurance) over three winters in black-capped chickadees Poecile atricapillus, American tree sparrows Spizella arborea, and dark-eyed juncos Junco hyemalis. For raw thermogenic endurance data, residuals of maximum cold-induced metabolic rate and thermogenic endurance from mass regressions were significantly and positively correlated in juncos and tree sparrows, and their correlation approached significance for chickadees. Log10 transformation of thermogenic endurance and mass data gave similar results. These data provide the first direct evidence for a phenotypic correlation between maximum cold-induced metabolic rate and thermogenic endurance in small birds, although much of the variance in thermogenic endurance is explained by factors other than maximum cold-induced metabolic rate and the degree of correlation differs among species. Nevertheless, these data suggest that physiological adjustments producing elevated thermogenic endurance also produce elevated maximum cold-induced metabolic rate in small birds.     

Anti-oxidant effects of cinnamon (Cinnamomum verum) bark and greater cardamom (Amomum subulatum) seeds in rats fed high fat diet

In order to gain insight into the antioxidant effect of cinnamon (Cinnamomum verum; Lauraceae) and cardamom (Amomum subulatum; Zingiberaceae) hepatic and cardiac antioxidant enzymes, glutathione (GSH) content and lipid conjugated dienes were studied in rats fed high fat diet along with cinnamon or cardamom. The antioxidant enzyme activities were found to be significantly enhanced whereas GSH content was markedly restored in rats fed a fat diet with spices. In addition, these spices partially counteracted increase in lipid conjugated dienes and hydroperoxides, the primary products of lipid peroxidation. Thus, it appears that these spices exert antioxidant protection through their ability to activate the antioxidant enzymes.     

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats.

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4 degrees C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24 degrees C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of beta- and alpha1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3'-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.     

Neuroprotection by Spice-Derived Nutraceuticals: You Are What You Eat!

Numerous lines of evidence indicate that chronic inflammation plays a major role in the development of various neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, brain tumor, and meningitis. Why these diseases are more common among people from some countries than others is not fully understood, but lifestyle factors have been linked to the development of neurodegenerative diseases. For example, the incidence of certain neurodegenerative diseases among people living in the Asian subcontinent, where people regularly consume spices, is much lower than in countries of the western world. Extensive research over the last 10 years has indicated that nutraceuticals derived from such spices as turmeric, red pepper, black pepper, licorice, clove, ginger, garlic, coriander, and cinnamon target inflammatory pathways, thereby may prevent neurodegenerative diseases. How these nutraceuticals modulate various pathways and how they exert neuroprotection are the focus of this review.     

TRPA1 Agonists—Allyl Isothiocyanate and Cinnamaldehyde—Induce Adrenaline Secretion

Thermosensitive transient receptor potential (TRP) channels, especially TRPV1 and TRPA1, are activated by the pungent compounds present in spices. TRPV1 activation by the intake of capsaicin, the irritant in hot pepper, induces adrenaline secretion and increases energy consumption. TRPV1 is mainly expressed in the sensory neurons and coexpressed with TRPA1 at a high frequency. However, the mechanism underlying adrenaline secretion by TRPA1 agonists such as allyl isothiocyanate (AITC) and cinnamaldehyde (CNA), the pungent ingredients in mustard and cinnamon, is not known. We examined whether AITC and CNA could induce adrenaline secretion in anesthetized rats. An intravenous injection of AITC or CNA (10 mg/kg) increased adrenaline secretion. These responses disappeared completely in capsaicin-treated rats with an impaired sensory nerve function. Moreover, pretreatment with cholinergic blockers (hexamethonium and atropine) attenuated the AITC- or CNA-induced adrenaline secretion. These results suggest that TRPA1 agonists activate the sensory nerves and induce adrenaline secretion via the central nervous system.     

Fungi and aflatoxins associated with spices in the Sultanate of Oman

One hundred and five samples of seven spices (cumin, cinnamon, clove, black pepper, cardamom, ginger, and coriander) were purchased from five popular companies in the Sultanate of Oman. The spices were surveyed for the mycoflora and aflatoxins. Twenty fungal species were isolated in which Aspergillus flavus , A. niger . Penicillium , Rhizopus , and Syncephalastrum racemosum were the most dominant. When colony forming units per gm (cfu/gm) of fungi were compared, significant differences were found among spices and companies. Of the seven spices studied, clove was found to be the least contaminated, while cumin was the most contaminated. None of the 15 selected samples of the spices contaminated by A. flavus were found to contain aflatoxins. Nevertheless, nine isolates (45%) of the twenty A. flavus strains screened for aflatoxins were aflatoxigenic. The moisture content of most of the spices was below the maximum standard limit. The results showed that the spices were contaminated by some fungi that might constitute health hazards for humans. This revised version was published online in June 2006 with corrections to the Cover Date.     

Thermoregulation in hypergravity-acclimated rats

To determine the effect of hypergravity acclimation on thermoregulation, core temperature (Tc), tail temperature (Tt), and O2 consumption (VO2) were measured in control rats (raised at 1 G) and in rats acclimated to 2.1 G. When the animals were exposed to a low ambient temperature of 9 degrees C, concurrently with a hypergravic field of 2.1 G, Tc of rats raised at 1 G fell markedly by approximately 6 degrees C (to 30.8 +/- 0.6 degrees C) while that of the rats raised at 2.1 G remained relatively constant (falling only approximately 1 degree C to 36.4 +/- 0.3 degrees C). Thus prior acclimation to a 2.1-G field enabled rats to maintain Tc when cold exposed in a 2.1-G field. To maintain Tc, thermogenic mechanisms were successfully activated in the 2.1-G-acclimated rats as shown by measurements of VO2. In contrast, VO2 measurements showed that rats reared at 1 G and then cold exposed at 2.1 G did not activate thermogenic mechanisms sufficiently to prevent a fall in Tc. In other experiments, rats acclimated to either 1 or 2.1 G were found to lack the ability to maintain their Tc when exposed to a 5.8-G field or when exposed to prolonged cold exposure at 1 G. Results are interpreted as showing that when placed in a 2.1-G field, rats acclimated to 2.1 G can more closely maintain their Tc near 37 degrees C when cold exposed than can rats acclimated to 1 G. However, this enhanced regulatory ability of 2.1-G-acclimated rats over 1.0-G-acclimated rats is restricted to 2.1-G fields and is not observed in 1.0- and 5.8-G fields.     

Thermogenic drinking: mediation by osmoreceptor and angiotensin II pathways

Exposure of rats to air at 5 C for 1-12 days is accompanied by a relative dehydration in spite of the continued presence of water. Dehydration during exposure to cold was manifested by: 1) a reduction in the ratio of water/food ingested; 2) an increase in the ratio of urine excreted/water ingested; 3) an increased evaporative water loss; 4) an increased serum osmolality and chloride concentration; and 5) a striking thirst and ingestion of water after transfer from cold to air at 26 C. Drinking began within 15 min and lasted approximately 1 h. Thermogenic drinking persisted for at least 120 days of exposure to cold. It was not thwarted by preventing access to water for either 1 or 2 h after transfer to warm air, but either intragastric or intraperitoneal administration of a water load equal to 3% of body weight inhibited water intake after transfer. These characteristics of thermogenic drinking are similar to those observed after 24 h of dehydration at 26 C; they also suggest that the cold-exposed rat is dehydrated relative to controls. These results suggest that osmoreceptors may play a role in the induction of thermogenic drinking. However, angiotensin II receptors may also play a role. Thermogenic drinking was inhibited by a beta 2-adrenergic, but not a beta 1-adrenergic, antagonist as well as by captopril, an inhibitor of the conversion of angiotensin I to angiotensin II. Further, plasma renin activity increased fourfold within 15 min after removal from cold. This suggests that an additional component involved in thermogenic drinking is the angiotensin II receptor. The extent to which thermogenic drinking is mediated by each pathway is unknown and will require additional studies.     

Acute cold exposure-induced down-regulation of CIDEA, cell death-inducing DNA fragmentation factor-α-like effector A, in rat interscapular brown adipose tissue by sympathetically activated β3-adrenoreceptors

The thermogenic activity of brown adipose tissue (BAT) largely depends on the mitochondrial uncoupling protein 1 (UCP1), which is up-regulated by environmental alterations such as cold. Recently, CIDEA (cell death-inducing DNA fragmentation factor-α-like effector A) has also been shown to be expressed at high levels in the mitochondria of BAT. Here we examined the effect of cold on the mRNA and protein levels of CIDEA in interscapular BAT of conscious rats with regard to the sympathetic nervous system. Cold exposure (4 °C for 3 h) elevated the plasma norepinephrine level and increased norepinephrine turnover in BAT. Cold exposure resulted in down-regulation of the mRNA and protein levels of CIDEA in BAT, accompanied by up-regulation of mRNA and protein levels of UCP1. The cold exposure-induced changes of CIDEA and UCP1 were attenuated by intraperitoneal pretreatment with propranolol (a non-selective β-adrenoreceptor antagonist) (2 mg/animal) or SR59230A (a selective β₃-adrenoreceptor antagonist) (2 mg/animal), respectively. These results suggest that acute cold exposure resulted in down-regulation of CIDEA in interscapular BAT by sympathetically activated β₃-adrenoreceptor-mediated mechanisms in rats.     

TRPA1 agonists--allyl isothiocyanate and cinnamaldehyde--induce adrenaline secretion

Thermosensitive transient receptor potential (TRP) channels, especially TRPV1 and TRPA1, are activated by the pungent compounds present in spices. TRPV1 activation by the intake of capsaicin, the irritant in hot pepper, induces adrenaline secretion and increases energy consumption. TRPV1 is mainly expressed in the sensory neurons and coexpressed with TRPA1 at a high frequency. However, the mechanism underlying adrenaline secretion by TRPA1 agonists such as allyl isothiocyanate (AITC) and cinnamaldehyde (CNA), the pungent ingredients in mustard and cinnamon, is not known. We examined whether AITC and CNA could induce adrenaline secretion in anesthetized rats. An intravenous injection of AITC or CNA (10 mg/kg) increased adrenaline secretion. These responses disappeared completely in capsaicin-treated rats with an impaired sensory nerve function. Moreover, pretreatment with cholinergic blockers (hexamethonium and atropine) attenuated the AITC- or CNA-induced adrenaline secretion. These results suggest that TRPA1 agonists activate the sensory nerves and induce adrenaline secretion via the central nervous system.     

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. Thyroid ablation was performed in normal rats after 2 mo of exposure to 4 degrees C, when BAT hypertrophy and thermogenic activity were maximal. After ablation, hypothyroid and normal controls remained in the cold for 2 additional months. At the end of the 4-mo cold exposure, all untreated hypothyroid rats were alive, had normal body temperature, and had gained an average 12.8% more weight than normal controls. Long-term cold exposure of hypothyroid rats markedly increased BAT weight, mitochondrial proteins, uncoupling protein (UCP)-1, mRNA for UCP-1, and oxygen consumption to levels similar to those seen in cold-exposed normal rats. The results indicate that thyroid hormones are required for increased thermogenic capacity to occur as an adaptation to long-term cold exposure. However, cold adaptation can be maintained in the absence of thyroid hormone.     

Nonshivering thermogenesis in a marsupial (the tasmanian bettong Bettongia gaimardi) is not attributable to brown adipose tissue

The Tasmanian bettong (Bettongia gaimardi, a marsupial) is a rat-kangaroo that increases nonshivering thermogenesis (NST) in response to norepinephrine (NE). This study attempted to assess whether brown adipose tissue (BAT), a specialized thermogenic effector, is involved in NST in the bettong. Regulatory NST, indicated by resting oxygen consumption (Vo2) of the whole body, was measured under conscious conditions at 20 degrees C with various stimuli: cold (4 degrees -5 degrees C) or warm (25 degrees C) acclimation, NE injection, and the beta3-adrenoceptor agonist (BRL) 37344. In line with the functional studies in vivo, the presence of BAT was evaluated by examining the expression of the uncoupling protein 1 (UCP1) with both rat cDNA and oligonucleotide probes. Both NE and BRL 37344 significantly stimulated NST in the bettong. After cold acclimation of the animals (at 4 degrees -5 degrees C for 2 wk), the resting Vo2 was increased by 15% and the thermogenic effect of NE was enhanced; warm-acclimated animals showed a slightly depressed response. However, no expression of UCP1 was detected in bettongs either before or after cold exposure (2 wk). These data suggest that the observed NST in the marsupial bettong is not attributable to BAT.     

Comparison between two rat sympathetic pathways activated in cold defense

In cold defense and fever, activity increases in sympathetic nerves supplying both tail vessels and interscapular brown adipose tissue (iBAT). These mediate cutaneous vasoconstrictor and thermogenic responses, respectively, and both depend upon neurons in the rostral medullary raphé. To examine the commonality of brain circuits driving these two outflows, sympathetic nerve activity (SNA) was recorded simultaneously from sympathetic fibers in the ventral tail artery (tail SNA) and the nerve to iBAT (iBAT SNA) in urethane-anesthetized rats. From a warm baseline, cold-defense responses were evoked by intermittently circulating cold water through a water jacket around the animal's shaved trunk. Repeated episodes of trunk skin cooling decreased core (rectal) temperature. The threshold skin temperature to activate iBAT SNA was 37.3 +/- 0.5 degrees C (n = 7), significantly lower than that to activate tail SNA (40.1 +/- 0.4 degrees C; P < 0.01, n = 7). A fall in core temperature always strongly activated tail SNA (threshold 38.3 +/- 0.2 degrees C, n = 7), but its effect on iBAT SNA was absent (2 of 7 rats) or weak (threshold 36.9 +/- 0.1 degrees C, n = 5). The relative sensitivity to core vs. skin cooling (K-ratio) was significantly greater for tail SNA than for iBAT SNA. Spectral analysis of paired recordings showed significant coherence between tail SNA and iBAT SNA only at 1.0 +/- 0.1 Hz. The coherence was due entirely to the modulation of both signals by the ventilatory cycle because it disappeared when the coherence spectrum was partialized with respect to airway pressure. These findings indicate that independent central pathways drive cutaneous vasoconstrictor and thermogenic sympathetic pathways during cold defense.     

Contribution of shivering and nonshivering thermogenesis to thermogenic capacity for the deer mouse (Peromyscus maniculatus)

Small mammals that are active all year must develop ways to survive the cold winters. Endotherms that experience prolonged cold exposure often increase their thermogenic capacity. Thermogenic capacity incorporates basal metabolic rate (BMR), nonshivering thermogenesis (NST), and shivering thermogenesis (ST). Increasing the capacity of any of these components will result in increased thermogenic capacity. It is often thought that NST should be the most plastic component of thermogenic capacity and as such is the most likely to increase with cold acclimation. We used deer mice to test this hypothesis by acclimating 27 animals to one of two temperatures (5 degrees or 22 degrees C) for 8 wk. We then measured and compared values for thermogenic capacity--BMR, ST, and NST--between the two groups. Thermogenic capacity and NST increased by 21% and 42%, respectively, after cold acclimation. Neither BMR nor ST showed any change after acclimation. Therefore, it appears that deer mice raise their thermogenic capacity in response to prolonged cold by altering NST only.     

Photoperiod and ambient temperature as environmental cues for seasonal thermogenic adaptation in the Djungarian hamster,Phodopus sungorus

For their seasonal control of thermogenesis Djungarian hamsters rely on environmental cueing by both photoperiod and ambient temperature. Their total potential for adaptive improvements of nonshivering thermogenesis is constant in summer and winter. The shortening of photoperiod in fall is used to anticipate about half of the total improvement in thermogenesis, in advance of any experience of cold, as can be concluded from the photoperiodic control of thermogenesis, cold resistance, and the protein content, cyctochrome oxidase activity and content of mitochondria in brown adipose tissue. The remainder of the seasonal thermogenic adaptation is due to stimulatory responses to chronic exposure to cold.This research was supported by the Deutsche Forschungsgemeinschaft, Schwerpunktprogramm Mechanismen der Temperaturregulation und -Adaptation.     

Role of photoperiod and melatonin in seasonal acclimatization of the djungarian hamster,Phodopus sungorus

The Djungarian hamster,Phodopus sungorus, shows a clear annual cycle in some thermogenic parameters such as nonshivering thermogenesis (NST) and cold resistance. These seasonal changes were found to be basically controlled by natural changes in photoperiod. Further support for this view was obtained by exposing the hamsters to artificial long and short photoperiods.Implantation of melatonin during fall and winter results in an increased thermogenic capacity in both short and long day hamsters comparable to that shown by values of control hamsters exposed to short photoperiods during winter. This thermotropic action of melatonin and of short photoperiod could be found only in fall and winter whereas during spring and summer, melatonin, like photoperiod, had no influence on thermogenic capacities. These results show that the actions of melatonin and photoperiod vary with the season and that they depend upon the photoperiodic history of the hamsters. Our results further indicate that the pineal gland with its hormone melatonin is involved in mediation of photoperiodic control of seasonal acclimatization.