Rodent hair is a Poor biomarker for internal manganese exposure.

Hair is used as a biomarker of manganese (Mn) exposure, yet there is limited evidence to support its utility to quantify internal vs external Mn exposure. C57BL/6 J mice and Sprague-Dawley rats were exposed in two blocks of 3 subcutaneous injections every 3 days starting on day 0 or 20. The control group received two blocks of saline (vehicle); Treatment A received the first block as Mn (50 mg/kg MnCl2 tetrahydrate), with the second block as either methylmercury (MeHg at 2.6 or 1.3 mg/kg) for mice or vehicle for rats; and Treatment B received Mn for both blocks. Hair was collected on days 0 and 60 from all treatment groups and Mn quantified by inductively coupled plasma-mass spectrometry (ICP-MS) and total Hg by Direct Mercury Analyzer (DMA). No correlation between internal Mn dose and hair Mn was observed, whereas hair Hg was significantly elevated in MeHg exposed vs non-exposed mice. Whole body Mn content at day 60 was quantified postmortem by neutron activation analysis, which detected significantly elevated Mn for Treatment B in mice and rats. Overall, we find no evidence to support the use of hair as a valid biomarker for internal exposure to Mn at a neurotoxic level.

In vitro antioxidant activities and inhibitory effects of phenolic extract of Senecio biafrae (Oliv and Hiern) against key enzymes linked with type II diabetes mellitus and Alzheimer's disease.

The phenolic extract of Senecio biafrae leaves was investigated to determine the in vitro antioxidant, phenolic profiles, and inhibition of key enzymes relevant to type II diabetes mellitus (α-amylase and α-glucosidase) and Alzheimer's disease (acetylcholinesterase and butrylcholinesterase). The phenolic extract demonstrated significant scavenging abilities against all in vitro antioxidant parameters assessed. Reversed-phase HPLC of the extract revealed the presence of gallic acid, chlorogenic, caffeic acid, rutin, quercetin, and kaempferol. The extract also inhibited activities of α-amylase (IC 50 = 126.90 µg/ml), α-glucosidase (IC 50 = 139.66 µg/ml), acetylcholinesterase (IC 50 = 347.22 µg/ml), and butrylcholinesterase (IC 50 = 378.79 µg/ml), which may be attributed to the antioxidant potential of the extract and its phenolic composition. Therefore, this study suggests that the leaves of S. biafrae may be useful in the management of diabetes mellitus and Alzheimer's disease.

C. elegans as a model in developmental neurotoxicology.

Due to many advantages Caenorhabditis elegans (C. elegans) has become a preferred model of choice in many fields, including neurodevelopmental toxicity studies. This review discusses the benefits of using C. elegans as an alternative to mammalian systems and gives examples of the uses of the nematode in evaluating the effects of major known neurodevelopmental toxins, including manganese, mercury, lead, fluoride, arsenic and organophosphorus pesticides. Reviewed data indicates numerous similarities with mammals in response to these toxins. Thus, C. elegans studies have the potential to predict possible effects of developmental neurotoxicants in higher animals, and may be used to identify new molecular pathways behind neurodevelopmental disruptions, as well as new toxicants.

Caffeic and chlorogenic acids inhibit key enzymes linked to type 2 diabetes (in vitro): a comparative study.

BACKGROUND: Chlorogenic acid is a major phenolic compound that forms a substantial part of plant foods and is an ester of caffeic acid and quinic acid. However, the effect of the structures of both chlorogenic and caffeic acids on their antioxidant and antidiabetic potentials have not been fully understood. Thus, this study sought to investigate and compare the interaction of caffeic acid and chlorogenic acid with α-amylase and α-glucosidase (key enzymes linked to type 2 diabetes) activities in vitro. METHODS: The inhibitory effect of the phenolic acids on α-amylase and α-glucosidase activities was evaluated. Thereafter, their antioxidant activities as typified by their 1,1-diphenyl-2 picrylhydrazyl radical scavenging ability and ferric reducing antioxidant properties were determined. RESULTS: The results revealed that both phenolic acids inhibited α-amylase and α-glucosidase activities in a dose-dependent manner (2-8 µg/mL). However, caffeic acid had a significantly (p<0.05) higher inhibitory effect on α-amylase [IC50 (concentration of sample causing 50% enzyme inhibition)=3.68 µg/mL] and α-glucosidase (IC50=4.98 µg/mL) activities than chlorogenic acid (α-amylase IC50=9.10 µg/mL and α-glucosidase IC50=9.24 µg/mL). Furthermore, both phenolic acids exhibited high antioxidant properties, with caffeic acid showing higher effects. CONCLUSIONS: The esterification of caffeic acid with quinic acid, producing chlorogenic acid, reduces their ability to inhibit α-amylase and α-glucosidase activities. Thus, the inhibition of α-amylase and α-glucosidase activities by the phenolic acids could be part of the possible mechanism by which the phenolic acids exert their antidiabetic effects.

Local salt substitutes "Obu-otoyo" activate acetylcholinesterase and butyrylcholinesterase and induce lipid peroxidation in rat brain.

Evidence has shown that ingestion of heavy metals can lead to neurodegenerative diseases. This study aimed to investigate the neurotoxic potential of salt substitutes (Obu-Otoyo); salt A (made by burning palm kernel shaft then soaked in water overnight and the extract from the resulting residue is used as the salt substitute) and salt B (an unrefined salt mined from a local site at Ilobu town, Osun-State, Nigeria) by assessing their effect on some key enzymes linked with neurodegenerative disease [acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities] as well as on malondialdehyde (MDA) content of the rat brain. Salt substitutes were fed to normal rats as dietary inclusion at doses of 0.5 and 1.0% for 30 days. Thereafter, the effect of the salt substitutes on AChE and BChE activities as well as on MDA level in the rat brain was determined. The results revealed that the salt substitutes caused a significant (p<0.05) increase in both AChE and BChE activity and also induced lipid peroxidation in the brain of rats in vivo as well as under in vitro condition in a dose-dependent manner. The effect of the salt substitutes on AChE and BChE activities could be attributed to the presence of some toxic heavy metals. Therefore, the ability of the salt substitutes to induce lipid peroxidation and activate AChE and BChE activities could provide some possible mechanism for their neurotoxic effect.

Anticholinesterase and Antioxidative Properties of Aqueous Extract of Cola acuminata Seed In Vitro.

Background. Cola acuminata seed, a commonly used stimulant in Nigeria, has been reportedly used for the management of neurodegenerative diseases in folklore without scientific basis. This study sought to investigate the anticholinesterase and antioxidant properties of aqueous extracts from C. acuminata seed in vitro. Methodology. The aqueous extract of C. acuminata seed was prepared (w/v) and its effect on acetylcholinesterase (AChE) and butyrylcholinesterase activities, as well as some prooxidant (FeSO4, sodium nitroprusside (SNP), and quinolinic acid (QA)) induced lipid peroxidation in rat brain in vitro, was investigated. Results. The results revealed that C. acuminata seed extract inhibited AChE (IC50 = 14.6 µg/mL) and BChE (IC50 = 96.2 µg/mL) activities in a dose-dependent manner. Furthermore, incubation of rat's brain homogenates with some prooxidants caused a significant increase P < 0.05 in the brain malondialdehyde (MDA) content and inhibited MDA production dose-dependently and also exhibited further antioxidant properties as typified by their high radicals scavenging and Fe(2+) chelating abilities. Conclusion. Inhibition of AChE and BChE activities has been the primary treatment method for mild Alzheimer's disease (AD). Therefore, one possible mechanism through which the seed exerts its neuroprotective properties is by inhibiting cholinesterase activities as well as preventing oxidative-stress-induced neurodegeneration. However, this is a preliminary study with possible physiological implications.

Inhibitory effect of polyphenolic-rich extract from Cola nitida (Kolanut) seed on key enzyme linked to type 2 diabetes and Fe(2+) induced lipid peroxidation in rat pancreas in vitro.

OBJECTIVE: To investigate the inhibitory effect of phenolic-rich extracts from Cola nitida (C. nitida) seeds on key enzymes linked with type-2 diabetes and Fe(2+) induced oxidative stress in rat pancreas. METHODS: The phenolic extract was prepared with 80% acetone (v/v). Subsequently, the antioxidant properties and inhibitory effect of the extract on α - amylase and α - glucosidase as well as on Fe(2+) induced lipid peroxidation in rat pancreas were determined in vitro. RESULTS: The result revealed that C. nitida extract inhibited α-amylase (EC50=0.34 mg/mL) and α-glucosidase (EC50=0.32 mg/mL) activities as well as Fe(2+) induced lipid peroxidation in rat pancreas in a dose dependent manner. In addition, the extract had high DPPH radical scavenging ability (EC50=2.2 mg/mL) and reducing power (8.2 mg AAE/g). Characterization of the main phenolic compounds of the extract using gas chromatography analysis revealed catechin (6.6 mg/100 g), epicatechin (3.6 mg/100 g), apigenin (5.1 mg/100 g) and naringenin (3.6 mg/100 g) were the main compounds in the extract. CONCLUSIONS: This antioxidant and enzyme inhibition could be some of the possible mechanism by which C. nitida is use in folklore for the management/treatment of type-2 diabetes. However, the enzyme inhibitory properties of the extract could be attributed to the presence of catechin, epicatechin, apigenin and naringenin.

Dietary inclusion of local salt substitutes induces oxidative stress and renal dysfunction in rats.

Our earlier report has shown that salt substitutes (Obu-Otoyo) contain some toxic heavy metals. This study, therefore, investigated the effect of the dietary inclusion of salt substitutes (Obu-Otoyo), namely, salt "A" and "B", on biomarkers of oxidative stress and renal function in rats. Salt "A", which has a gray color, is the product of a process in which ash is produced by burning palm kernel shaft soaked in water overnight and extracting the residue to produce the salt substitute while Salt "B", which has a white color, is a rock salt mined from a local site at Ilobu town, Osun-State, Nigeria. Salt substitutes were fed to normal rats as dietary inclusion at 0.5% and 1.0% for 21 days. The dietary inclusion of the salt substitutes caused a significant (p<0.05) increase in plasma activities of creatinine, urea, uric acid, and blood urea nitrogen compared with the control. Meanwhile, the dietary inclusion of the salt substitutes caused a significant (p<0.05) decrease in renal superoxide dismutase, catalase, reduced glutathione level, glutathione-S-transferase, and glutathione peroxidase activities with a concomitant increase in the malondialdehyde level compared with the control. Furthermore, there was a significant (p<0.05) increase in the concentrations of heavy metals, such as Pb, Co, Cu, Fe, Zn and Cr, in kidney of rats fed with the salt substitute Obu-Otoyo. Therefore, this finding indicates that Obu-Otoyo induces nephrotoxicity in rats. The nephrotoxicity of Obu-Otoyo could be attributed to the induction of oxidative stress as a result of the presence of some heavy metals, suggesting possible health hazards in subjects who consume it.

Phenolic Acids (Gallic and Tannic Acids) Modulate Antioxidant Status and Cisplatin Induced Nephrotoxicity in Rats.

Cisplatin (cis-diamminedichloroplatinum (II) or CDDP), used in the treatment of many solid-tissue cancers, has its chief side-effect in nephrotoxicity. Hence, this study sought to investigate and compare the protective effect of gallic acid (GA) and tannic acid (TA) against cisplatin induced nephrotoxicity in rats. The rats were given a prophylactic treatment of GA and TA orally at a dose of 20 and 40 mg/kg body weight for 7 consecutive days before the administration of a single intraperitoneal (i.p.) injection of cisplatin (CP) at 7.5 mg/kg bwt. The protective effects of both GA and TA on CP induced nephrotoxicity were investigated by assaying renal function, oxidative stress biomarkers, and histopathological examination of kidney architecture. A single dose of cisplatin (7.5 mg/kg bwt) injected i.p. caused a significant increase in some biomarkers of renal function (creatinine, uric acid, and urea levels), with a marked elevation in malondialdehyde (MDA) content accompanied by a significant (P < 0.05) decrease in reduced glutathione (GSH) content (103.27%) of kidney tissue as compared to control group. Furthermore, a significant (P < 0.05) reduction in kidney antioxidant enzymes (SOD, catalase, GPx, and GST) activity was observed. However, pretreatment with oral administration of tannic acid and gallic acid at a dose of 20 and 40 mg/kg body weight, respectively, for 7 days prior to cisplatin administration reduced histological renal damage and suppressed the generation of ROS, lipid peroxidation, and oxidative stress in kidney tissues. These results indicate that both gallic and tannic acids could serve as a preventive strategy against cisplatin induced nephrotoxicity.

Inhibition of key enzymes linked to type 2 diabetes and sodium nitroprusside-induced lipid peroxidation in rat pancreas by water-extractable phytochemicals from unripe pawpaw fruit (Carica papaya).

BACKGROUND: Various parts of unripe pawpaw (Carica papaya Linn) fruit have been reportedly used for the management or treatment of diabetes mellitus in folklore medicine. Therefore, the present study sought to investigate the inhibitory effects of the aqueous extract of different parts of unripe pawpaw fruit on key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) and sodium nitroprusside (SNP)-induced lipid peroxidation in rat pancreas in vitro. METHODS: The aqueous extracts of the unripe pawpaw (C. papaya) fruit parts were prepared (1:20 w/v) and the ability of the extracts to inhibit α-amylase, α-glucosidase and SNP-induced lipid peroxidation in rat pancreas in vitro was investigated. RESULTS: The results revealed that all the extracts inhibited α-amylase (IC50=0.87-1.11 mg/mL), α-glucosidase (IC50=1.76-2.64 mg/mL) and SNP-induced lipid peroxidation (IC50=1.99-2.42 mg/mL) in a dose-dependent manner. However, combination of the flesh, seed and peel in equal amounts had the highest inhibitory effect on α-amylase and α-glucosidase activities. CONCLUSIONS: Strong inhibitory activities of the unripe pawpaw fruit against key enzymes linked to type 2 diabetes and SNP-induced lipid peroxidation in rat pancreas could be part of the mechanism by which unripe pawpaw is used in the management/prevention of diabetes mellitus in folk medicine. However, combining the unripe pawpaw fruit parts in equal amounts exhibited synergistic properties on α-amylase and α-glucosidase inhibitory activities.

Aqueous extracts of two varieties of ginger (Zingiber officinale) inhibit angiotensin I-converting enzyme, iron(II), and sodium nitroprusside-induced lipid peroxidation in the rat heart in vitro.

Ginger has reportedly been used in folk medicine for the management and prevention of hypertension and other cardiovascular diseases. Therefore, this study sought to investigate the inhibitory effect of aqueous extracts of two varieties of ginger on a key enzyme linked to hypertension (angiotensin I-converting enzyme [ACE]), and on pro-oxidants [Fe(2+) and sodium nitroprusside (SNP)] which have been shown to induce lipid peroxidation in the rat's isolated heart in vitro. Aqueous extracts (0.05 mg/mL) of red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe) were prepared and the ability of the extracts to inhibit ACE along with Fe(2+)- and SNP-induced lipid peroxidation was determined in rat's heart in vitro. Results revealed that both extracts inhibited ACE in a dose-dependent manner (25-125 µg/mL). However, red ginger extract (EC50=27.5 µg/mL) had a significantly (P<.05) higher inhibitory effect on ACE than white ginger extract (EC50=87.0 µg/mL). Furthermore, incubation of the rat's heart in the presence of Fe(2+) and SNP caused a significant increase (P<.05) in the malondialdehyde (MDA) content of the heart homogenates, while the introduction of the ginger extracts (78-313 µg/mL) caused a dose-dependent decrease in the MDA content of the stressed heart homogenates. This suggests that the possible mechanism through which ginger exerts its antihypertensive properties may be through inhibition of ACE activity and prevention of lipid peroxidation in the heart. Furthermore, red ginger showed stronger inhibition of ACE than white ginger. Additionally, it should be noted that these protective properties of the ginger varieties could be attributed to their polyphenol contents.

Inhibitory Effect of Phenolic Extract from Garlic on Angiotensin-1 Converting Enzyme and Cisplatin induced Lipid Peroxidation - In Vitro.

Allium sativum have been an important food ingredient in the management or treatment of renal disease. Therefore, this study sought to determine the inhibitory effect of phenolic-rich extract from A. sativum on angiotensin 1 converting enzyme (ACE) activity (key enzyme linked to renal dysfunction) and cisplatin-induced lipid peroxidation in rat kidney in vitro. The free phenolics were extracted with 80% acetone, while the bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate. Thereafter, their inhibitory effect on angiotensin 1 converting enzyme (ACE) activity and cisplatin-induced lipid peroxidation in rat kidney were determined-in vitro. The results revealed that the free phenolics had significantly higher (P<0.05) inhibitory effect on ACE activity than the bound phenolics. Furthermore, incubation of rat kidney in presence of 1 mM cisplatin caused a significant increase (P<0.05) in the malondialdehyde (MDA) content, however, both extracts inhibited MDA produced in a dose dependent manner. The additive and/or synergistic action of the free and bound phenolics could have contributed to the observed medicinal properties of the spice. Therefore, inhibition of ACE activity and prevention of oxidative stress in the kidney could be some of the possible mechanism by which they exert nephroprotective properties. However, the bound phenolic extracts showed stronger inhibition on ACE activity in vitro.

Inhibitory effect of aqueous extract of different parts of unripe pawpaw (Carica papaya) fruit on Fe²âº-induced oxidative stress in rat pancreas in vitro.

CONTEXT: Carica papaya L. (Caricaceae) is widespread throughout tropical Africa; it is cultivated for its fruits and it is eaten in various ways. OBJECTIVE: This study sought to investigate the inhibitory effect of the aqueous extract of different parts of unripe pawpaw fruit on Fe²âº-induced lipid peroxidation in rat's pancreas in vitro. MATERIALS AND METHODS: The aqueous extract of the unripe pawpaw fruit parts; peel (PG), seed (SG), flesh (FG), flesh with peel (FPG) and a combination of equal amount of all parts (CG) were prepared, the total phenolic content and the antioxidant activities of the extracts were then evaluated using various spectrophotometric methods. RESULT: PG had the highest total phenol content (1.24 mg GAE/g), flavonoid content (0.63 mg QUE/g), reducing power (7.07 mg AAE/g) and Fe²âº chelating ability while the SG had the highest 1,1-diphenyl-2-picrylhydrazyl radical scavenging ability. Furthermore, all the extracts caused a significant decrease (p < 0.05) in the malondialdehyde contents in the pancreas with SG (IC50 = 4.25 mg/mL) having the highest inhibitory effect on Fe²âº-induced lipid peroxidation. DISCUSSION AND CONCLUSION: This protective effect of the extracts on Fe²âº-induced lipid peroxidation in rat pancreas could be attributed to their phenolic compounds and, the possible mechanism may be through their antioxidant activities. However, the effect of combination of different parts of unripe pawpaw fruit in equal amount (w/w) on the inhibition of Fe²âº-induced lipid peroxidation in rat pancreas exhibited additive properties.

Inhibitory Effect of Aqueous Extract of Stem Bark of Cissus populnea on Ferrous Sulphate- and Sodium Nitroprusside-Induced Oxidative Stress in Rat's Testes In Vitro.

Cissus populnea are plants associated with a myriad of medicinal uses in different parts of the world and are good sources of carotenoids, triterpenoids, and ascorbic acid. The antioxidant properties and inhibitory effect of water extractible phytochemicals from stem bark of C. populnea on FeSO(4) and sodium nitroprusside- (SNP-) induced lipid peroxidation in rat testes were investigated in vitro. The results revealed that the extract was able to scavenge DPPH radical, chelate Fe(2+) and also had a high reducing power. Furthermore, the incubation of the testes tissue homogenate in the presence of FeSO(4) and SNP, respectively, caused a significant increase in the malondialdehyde (MDA) contents of the testes. However, the aqueous extract of the stem bark of C. populnea caused a significant decrease in the MDA contents of both Fe(2+) (EC(50) = 0.027 mg/mL) and SNP- (EC(50) = 0.22 mg/mL) induced lipid peroxidation in the rat testes homogenates in a dose-dependent manner. The water extractible phytochemicals from C. populnea protect the testes from oxidative stress and this could be attributed to their high antioxidant activity: DPPH-scavenging ability, Fe(2+)-chelating and -reducing power. Therefore, oxidatively stress in testes could be potentially managed/prevented by this plant.

Anthocyanin - Rich Red Dye of Hibiscus Sabdariffa Calyx Modulates Cisplatin-induced Nephrotoxicity and Oxidative Stress in Rats.

This study sought to investigate the protective effect of dietary inclusion of Hibiscus sabdariffa calyx red dye on cisplatin-induced nephrotoxicity and antioxidant status in rats. Adult male rats were randomly divided into four groups of six animals each. Groups I and II were fed basal diet while groups III and IV were fed diets containing 0.5% and 1% of the dye respectively for 20 days prior to cisplatin administration. Nephrotoxicity was induced by a single dose intraperitoneal administration of cisplatin (7 mg/kg b.w) and the experiment was terminated 3 days after. The kidney and plasma were studied for nephrotoxicity and oxidative stress indices. Cisplatin administration caused a significant (P<0.05) increase in creatinine, uric acid, urea, and blood urea nitrogen (BUN) levels as well as kidney malondialdehyde (MDA) content, with concomitant decrease in kidney vitamin C and GSH contents. Furthermore, activities of kidney antioxidant enzymes such as, SOD, Catalase, and GST were significantly (P<0.05) altered in cisplatin administered rats. However, consumption of diets supplemented with the dye for 20 days prior to cisplatin administration protected the kidney and attenuates oxidative stress through modulation of in vivo antioxidant status. The determined anthocyanin content of the dye is 121.5 mg Cyanidin-3-rutinoside equivalent/100 g, thus, the observed nephroprotective effect of H. sabdariffa dye could be attributed to its anthocyanin content.

Comparative study on the inhibitory effect of caffeic and chlorogenic acids on key enzymes linked to Alzheimer's disease and some pro-oxidant induced oxidative stress in rats' brain-in vitro.

This study sought to investigate and compare the interaction of caffeic acid and chlorogenic acid on acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), and some pro-oxidants (FeSO(4), sodium nitroprusside and quinolinic acid) induced oxidative stress in rat brain in vitro. The result revealed that caffeic acid and chlorogenic acid inhibited AChE and BChE activities in dose-dependent manner; however, caffeic acid had a higher inhibitory effect on AChE and BChE activities than chlorogenic acid. Combination of the phenolic acids inhibited AChE and BChE activities antagonistically. Furthermore, pro-oxidants such as, FeSO(4), sodium nitroprusside and quinolinic acid caused increase in the malondialdehyde (MDA) contents of the brain which was significantly decreased dose-dependently by the phenolic acids. Inhibition of AChE and BChE activities slows down acetylcholine and butyrylcholine breakdown in the brain. Therefore, one possible mechanism through which the phenolic acids exert their neuroprotective properties is by inhibiting AChE and BChE activities as well as preventing oxidative stress-induced neurodegeneration. However, esterification of caffeic acid with quinic acid producing chlorogenic acid affects these neuroprotective properties.

Effect of dietary inclusion of salt substitutes "Obu-Otoyo" on some biochemical indices in rat.

"Obu-Otoyo" in folklore has been used as salt substitutes in diet of patients for the management of hypertension with no report on its toxicological effects. Hence, this study sought to investigate the effect of dietary inclusion of two types of the salt substitutes (Obu-Otoyo): salt A and salt B on some biochemical indices in rats. The mineral content of the salt substitutes was determined and the salt substitutes were fed to normal rats as dietary inclusion (0.1-1.0%). The dietary inclusion of the salt substitutes caused a significant (P<0.05) increase in plasma activities of alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin, and atherogenic lipids content (total cholesterol, LDL-cholesterol and triglyceride) with a concomitant decrease in the HDL-cholesterol content when compared with the control. Furthermore, the mineral determination of the salt substitutes revealed the presence of some toxic metals. The alterations in plasma activities of liver function enzymes and lipid profile in rat fed dietary inclusions of "Obu-Otoyo" may be related to the high content of some toxic/heavy metals in the salt substitutes. Therefore, this finding indicates that Obu-Otoyo is toxic to rat.

Antioxidant and inhibitory effect of red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe) on Fe(2+) induced lipid peroxidation in rat brain in vitro.

Neurodegerative diseases have been linked to oxidative stress arising from peroxidation of membrane biomolecules and high levels of Fe have been reported to play an important role in neurodegenerative diseases and other brain disorder. Malondialdehyde (MDA) is the end-product of lipid peroxidation and the production of this aldehyde is used as a biomarker to measure the level of oxidative stress in an organism. The present study compares the protective properties of two varieties of ginger [red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe)] on Fe(2+) induced lipid peroxidation in rat brain in vitro. Incubation of the brain tissue homogenate in the presence of Fe caused a significant increase in the malondialdehyde (MDA) contents of the brain. However, the aqueous extract from both varieties of ginger caused a significant decrease in the MDA contents of the brain in a dose-dependent manner. However, the aqueous extract of red ginger had a significantly higher inhibitory effect on both Fe(2+)-induced lipid peroxidation in the rat brain homogenates than that of white ginger. This higher inhibitory effect of red ginger could be attributed to its significantly higher phytochemical content, Fe(2+) chelating ability, OH scavenging ability and reducing power. However, part of the mechanisms through which the extractable phytochemicals in ginger (red and white) protect the brain may be through their antioxidant activity, Fe(2+) chelating and OH scavenging ability. Therefore, oxidative stress in the brain could be potentially managed/prevented by dietary intake of ginger varieties (red ginger and white ginger rhizomes).

Inhibition of acetylcholinesterase activities and some pro-oxidant induced lipid peroxidation in rat brain by two varieties of ginger (Zingiber officinale).

Ginger has been reportedly used for the management or treatment of Alzheimer's disease in folklore medicine. Therefore, this study sought to investigate the inhibitory effects of water extractable phytochemicals of red and white ginger on acetylcholinesterase activities, and sodium nitroprusside (SNP) and quinolinic acid (QA)-induced lipid peroxidation in rat brain -in vitro. Both extracts inhibited acetylcholinesterase (AChE) activities in a dose-dependent manner; however, white ginger had higher acetylcholinesterase inhibitory activity than red ginger. Combination of the ginger inhibited acetylcholinesterase activities synergistically. Furthermore, SNP and QA caused a significant increase in the malondialdehyde (MDA) contents of the brain; however, the extracts significantly decrease the SNP and QA elevated brain MDA contents in a dose-dependent manner. Nevertheless, there was no significant difference (P>0.05) in the inhibition of the SNP and QA-induced lipid peroxidation by both extracts. The inhibitory effect of ginger extracts on acetylcholinesterase activities and some prooxidants induced lipid peroxidation in rat's brain could be attributed to the presence of phytochemicals such as flavonoids, tannins, alkaloids and terpenoids. Therefore, some possible mechanism by which ginger extracts exert anti-Alzheimer properties could be through the inhibition of acetylcholinesterase activities and prevention of lipid peroxidation in the brain.

Attenuation of gentamycin-induced nephrotoxicity in rats by dietary inclusion of ginger (Zingiber officinale) and turmeric (Curcuma longa) rhizomes.

This study sought to investigate the modulatory effects of dietary inclusion of ginger (Zingiber officinale) and turmeric (Curcuma longa) rhizomes on antioxidant status and renal damage induced by gentamycin in rats. Renal damage was induced in albino rats pretreated with dietary inclusion of ginger and turmeric (2% and 4%) by intraperitoneal (i.p.) administration of gentamycin (100 mg/kg body weight) for three days. Assays for renal damage biomarkers (plasma creatinine, plasma urea, blood urea nitrogen and plasma uric acid), malondialdehyde (MDA) content and reduced glutathione (GSH) content as well as renal antioxidant enzymes (catalase, glutathione-S-transferase (GST), glutathione peroxidase (GPx) and superoxide dismutase (SOD)) were carried out. The study revealed significant (p < 0.05) increases in renal damage biomarkers following gentamycin administration with severe alteration in kidney antioxidant status. However, pretreatment with ginger and turmeric rhizome (2% and 4%) prior to gentamycin administration significantly (p < 0.05) protected the kidney and attenuated oxidative stress by modulating renal damage and antioxidant indices. This finding therefore suggests that dietary inclusion of ginger and turmeric rhizomes may protect against gentamycin-induced nephrotoxicity and oxidative stress.