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Protective effects of fruit extracts of Hippophae rhamnoides L. against arsenic toxicity in Swiss albino mice.

Seabuckthorn (Hippophae rhamnoides L.) berry has a long history of applications as a food and medicinal ingredient in eastern countries. The present study was carried out to investigate the effect of different fruit extracts of H. rhamnoides on altered biochemical parameters indicative of haematological alterations, tissue oxidative stress, and arsenic concentration in arsenic-exposed mice (2.5 mg/kg body weight, intraperitoneally). Two aqueous extracts (at room temperature and under reflux condition) and an ethanolic extract of H. rhamnoides at a dose of 500 mg/kg body weight were co-administered daily during arsenic exposure in mice for 3 weeks. Exposure to arsenic led to a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity, suggesting disturbed haem synthesis pathway. Arsenic also caused significant depletion of reduced hepatic glutathione (GSH) level, glutathione S-transferase (GST) and glutathione peroxidase and catalase activities, while it increased the level of thiobarbituric acid reactive substance (TBARS), suggesting liver oxidative stress. Most of the altered biochemical variables responded favorably to the co-supplementation of H. rhamnoides, particularly the aqueous fruit extract, extracted at room temperature (HF-WRT). However, arsenic concentration in blood and tissues remained unchanged, suggesting the lack of chelating property of fruit extract of H. rhamnoides. The present study, thus, led us to conclude that the fruit extract of H. rhamnoides has a significant protective role against arsenic-induced oxidative injury. However, it lacks the ability to remove arsenic from the binding sites, suggesting that the herbal extract could be co-administered with a chelating agent of known efficacy during treatment of arsenic to achieve the optimum effect of chelation treatment.

Animals↗

Arsenic-related Bowen's disease, palmar keratosis, and skin cancer.

Chronic arsenical intoxication can still be found in environmental and industrial settings. Symptoms of chronic arsenic intoxication include general pigmentation or focal "raindrop" pigmentation of the skin and the appearance of hyperkeratosis of the palms of the hands and soles of the feet. In addition to arsenic-related skin diseases including keratosis, Bowen's disease, basal-cell-carcinoma, and squamous-cell carcinoma, there is also an increased risk of some internal malignancies. Arsenic-related diseases are common in areas of the world where the drinking water has a high arsenic content. In this paper, we describe a 35-year-old male patient who had arsenic-related keratosis, squamous-cell carcinoma in the palmar area of his left hand, and Bowen's disease on his left thigh. The patient worked in a borax mine for 15 years, so he was exposed to arsenic in drinking water, airborne arsenic in his workplace, and had direct contact. The patient was treated for 11 months for arsenic-related keratosis until an axillary lymph node metastasis occurred; the lesion was excised and diagnosed to be malignant. Bowen's disease was detected when the patient was being treated for cancer. No other malignancy was found. The patient is still receiving regular follow-up care.

Adult↗

Profile of urinary arsenic metabolites during pregnancy.

Chronic exposure to inorganic arsenic (In-As) from drinking water is associated with different health effects, including skin, lung, bladder, and kidney cancer as well as vascular and possibly reproductive effects. In-As is metabolized through the process of methylation, resulting in the production and excretion of methylated species, mainly monomethylarsenate (MMA) and dimethylarsenate (DMA). Because a large percentage of the dose is excreted in urine, the distribution of urinary In-As, MMA, and DMA is considered a useful indicator of methylation patterns in human populations. Several factors affect these patterns, including sex and exposure level. In this study, we investigated the profile of urinary In-As, MMA, and DMA of pregnant women. Periodic urine samples were collected from early to late pregnancy among 29 pregnant women living in Antofagasta, Chile, who drank tap water containing 40 micro g/L In-As. The total urinary arsenic across four sampling periods increased with increasing weeks of gestation, from an initial mean value of 36.1 to a final value of 54.3 micro g/L. This increase was mainly due to an increase in DMA, resulting in lower percentages of In-As and MMA and a higher percentage of DMA. Our findings indicate that among women exposed to moderate arsenic from drinking water during pregnancy, changes occur in the pattern of urinary arsenic excretion and metabolite distribution. The toxicologic significance of this is not clear, given recent evidence suggesting that intermediate methylated species may be highly toxic. Nevertheless, this study suggests that arsenic metabolism changes throughout the course of pregnancy, which in turn may have toxicologic effects on the developing fetus. Key words: arsenic, arsenic metabolism, arsenic methylation, Chile, pregnancy, urinary arsenic.

Adult↗

Nutritional factors and susceptibility to arsenic-caused skin lesions in West Bengal, India.

There has been widespread speculation about whether nutritional deficiencies increase the susceptibility to arsenic health effects. This is the first study to investigate whether dietary micronutrient and macronutrient intake modulates the well-established human risk of arsenic-induced skin lesions, including alterations in skin pigmentation and keratoses. The study was conducted in West Bengal, India, which along with Bangladesh constitutes the largest population in the world exposed to arsenic from drinking water. In this case-control study design, cases were patients with arsenic-induced skin lesions and had < 500 microg/L arsenic in their drinking water. For each case, an age- and sex-matched control was selected from participants of a 1995-1996 cross-sectional survey, whose drinking water at that time also contained < 500 microg/L arsenic. Nutritional assessment was based on a 24-hr recall for major dietary constituents and a 1-week recall for less common constituents. Modest increases in risk were related to being in the lowest quintiles of intake of animal protein [odds ratio (OR) = 1.94; 95% confidence interval (CI), 1.05-3.59], calcium (OR = 1.89; 95% CI, 1.04-3.43), fiber (OR = 2.20; 95% CI, 1.15-4.21), and folate (OR = 1.67; 95% CI, 0.87-3.2). Conditional logistic regression suggested that the strongest associations were with low calcium, low animal protein, low folate, and low fiber intake. Nutrient intake was not related to arsenic exposure. We conclude that low intake of calcium, animal protein, folate, and fiber may increase susceptibility to arsenic-caused skin lesions. However, in light of the small magnitude of increased risks related to these dietary deficiencies, prevention should focus on reducing exposure to arsenic.

Adult↗

The effect of arsenic mitigation interventions on disease burden in Bangladesh.

Many interventions have been advocated to mitigate the impact of arsenic contamination of drinking water in Bangladesh. However, there are few data on the true magnitude of arsenic-related disease in Bangladesh nationally. There has also been little consideration given to possible adverse effects of such interventions, in particular, diarrheal disease. The purpose of this study was to estimate and compare the likely impacts of arsenic mitigation interventions on both arsenic-related disease and water-borne infectious disease. We found that arsenic-related disease currently results in 9,136 deaths per year and 174,174 disability-adjusted life years (DALYs; undiscounted) lost per year in those exposed to arsenic concentrations > 50 microg/L. This constitutes 0.3% of the total disease burden in Bangladesh in terms of undiscounted DALYs. We found intervention to be of overall benefit in reducing disease burden in most scenarios examined, but the concomitant increase in water-related infectious disease significantly reduced the potential benefits gained from intervention. A minimum reduction in arsenic-related DALYs of 77% was necessary before intervention achieved any reduction in net disease burden. This is assuming that interventions were provided to those exposed to > 50 microg/L and would concomitantly result in a 20% increase in water-related infectious disease in those without access to adequate sanitation. Intervention appears to be justified for those populations exposed to high levels of arsenic, but it must be based on exposure levels and on the effectiveness of interventions not only in reducing arsenic but in minimizing risk of water-related infections. Key words: arsenic/adverse effects, Bangladesh, burden of disease, diarrhea, risk assessment, water pollutants, water supply.

Adolescent↗

Changes in the chemical speciation of arsenic following ingestion by man.

The concentrations of four chemical species of arsenic in urine were observed with time, after ingestion of three different chemical species of arsenic. The arsenic-rich substances ingested, including arsenite-rich wine, arsenate-rich drinking water, and crab meat which contained organo-arsenic compounds. After ingestion of arsenite-rich wine, approximately 10% of the arsenic was excreted as arsenite, but the majority of the arsenic was methylated to methylarsonic acid and dimethylarsinic acid and excreted. After ingestion of arsenate-rich water, elevated levels of both arsenate and dimethylarsinic acid were observed. When crab meat was ingested, none of these four arsenic species were observed at elevated levels until the urine was heated in 2N NaOH. After the hot base digestion, high levels of dimethylarsinic acid were detected in these samples. The apparent biological half-lives were on the order of 10 hr for inorganic arsenic and 30 hr for the methylated arsenic forms.

Arsenic↗

Biomarkers of exposure: a case study with inorganic arsenic.

The environmental contaminant inorganic arsenic (iAs) is a human toxicant and carcinogen. Most mammals metabolize iAs by reducing it to trivalency, followed by oxidative methylation to pentavalency. iAs and its methylated metabolites are primarily excreted in urine within 4-5 days by most species and have a relatively low rate of bioaccumulation. Intra- and interindividual differences in the methylation of iAs may affect the adverse health effects of arsenic. Both inorganic and organic trivalent arsenicals are more potent toxicants than pentavalent forms. Several mechanisms of action have been proposed for arsenic-induced toxicity, but a scientific consensus has not been achieved. Biomarkers of exposure may be used to quantify exposure to iAs. The most common biomarker of exposure for iAs is the measurement of total urinary arsenic. However, consumption of seafood containing high concentrations of organic arsenic can confound estimation of iAs exposure. Because these organic species are thought to be relatively nontoxic, their presence in urine may not represent increased risk. Speciation of urinary arsenic into inorganic and organic forms, and even oxidation state, gives a more definitive indication of the exposure to iAs. Questions still remain, however, as to how reliably the measurement of urinary arsenic, either total or speciated, may predict arsenic concentrations at target tissues as well as how this measurement could be used to assess chronic exposures to iAs.

Animals↗

Arsenic increased lipid peroxidation in rat tissues by a mechanism independent of glutathione levels.

The role of lipid peroxidation in the mechanism of arsenic toxicity was investigated in female rats pretreated with N-acetylcysteine (NAC, a glutathione [GSH] inducer) or with buthionine sulfoximine (BSO, a GSH depletor). Rats were challenged with sodium arsenite, and sacrificed 1 hr after this treatment. Results showed that arsenic decreased GSH levels and increased lipid peroxidation in liver, kidney, and heart, with a larger effect at 18.2 mg/kg than at 14.8 mg/kg for lipid peroxidation induction. In the liver of rats treated with arsenic, pretreatment with NAC increased the levels of GSH and decreased lipid peroxidation. In kidney and heart, NAC pretreatment protected the tissues against arsenic-induced depletion of GSH levels, but the same degree of protection was not found for lipid peroxidation induction. In its turn, BSO had an additive effect with arsenic in lowering the levels of GSH in the liver and kidney, but an inverse correlation between GSH levels and lipid peroxidation was found only in liver. Arsenic content in tissues of rats pretreated with NAC was lower than in rats treated only with arsenic. In rats with depleted levels of GSH (BSO-pretreated rats), a shift in arsenic tissue distribution was found, with higher levels in skin and lower levels in kidney. A clear tendency for a positive correlation between arsenic concentration and lipid peroxidation levels was found in liver, kidney, and heart.

Acetylcysteine↗

Manganese enhances peroxynitrite and leukotriene E4 formation in bovine aortic endothelial cells exposed to arsenic.

Long-term exposure to arsenic in drinking water has been linked to cancer and other health effects, including cardiovascular disease. Arsenic in the environment is found in combination with a range of metals that could influence its toxicity. Manganese, in particular, is a metal that is typically found in conjunction with arsenic in contaminated groundwater. Peroxynitrite is a powerful oxidant formed from the reaction between nitric oxide and superoxide anion. Arsenic has been shown to increase the formation of peroxynitrite in bovine aortic endothelial cells (BAECs) and promote the formation of 3-nitrotyrosine (3-NY) in the atherosclerotic plaque of ApoE-/-/LDLr-/- mice. Arsenic exposure also increases leukotriene E4 (LTE4) formation in both the mice and BAECs, an effect that is partially reversed by the addition of Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor. In the present study, we investigated the effect of adding nontoxic concentrations of manganese along with arsenic to BAEC cultures. Manganese increased arsenic toxicity and enhanced peroxynitrite, 3-NY, and LTE4 formation in BAECs. Addition of LNAME reduced 3-NY formation induced by arsenic/manganese mixtures, but in contrast to its effect on arsenic alone, L-NAME actually increased LTE4 synthesis in BAECs treated with the arsenic/manganese combination. Overall, these data suggest that manganese may exacerbate the toxic effects of arsenic on the vascular system.

Animals↗

Merkel cell carcinoma in patients with long-term ingestion of arsenic.

Merkel cell carcinoma (MCC) is a rare primary neuroendocrine carcinoma of the skin, mostly occurring late in life on sun-exposed body parts. Little is known about the specific etiological factors in the pathogenesis of MCC. A previous report indicated that arsenic exposure might cause MCC, which might be another specific type of skin cancer associated with arsenic exposure. On the southwest coast of Taiwan, high arsenic levels in artesian well water have been documented, and various diseases associated with arsenic exposure have been found to be prevalent in this area. We report two pathologically confirmed cases of MCC in patients who had histories of long-term ingestion of arsenic from drinking water. The tumors were on the anterior chest wall, an area less exposed to the sun, in both cases. The literature on the dose-response relationship between arsenic exposure and MCC is limited. We estimated that the total arsenic ingested by these two cases was around 14.7 and 2.6 gm, respectively. We also tried to assess the cancer risk on the basis of the estimated doses of arsenic exposure and the cancer risk model developed by the U.S. Environmental Protection Agency (EPA). The estimated lifetime target cancer risk was 1.3 x 10(-2) in Case 1 and 2.3 x 10(-3) in Case 2. Both are much higher than the 10(-6) upper limit on lifetime cancer risk put forth by the U.S. EPA health protection standard. We believe that arsenic intoxication played an important role in the carcinogenic process of MCC in our cases.

Aged↗

Arsenic distribution in Florida urban soils: comparison between Gainesville and Miami.

Arsenic contamination is of concern due to its effect as a carcinogen. Understanding the distribution of arsenic in urban soils is important for establishing baseline concentrations from which anthropogenic effects can be measured. The soil cleanup target level (SCTL) for arsenic in Florida (0.8 and 3.7 mg kg(-1) in residential and commercial areas, respectively) is lower than in most states and is near the arsenic background concentrations in Florida soils. The objective of this study was to characterize the distribution of arsenic in the soils of two Florida cities, Gainesville and Miami. More than 200 soil samples were collected from three land-use classes in each city (residential, commercial, and public land), digested with USEPA Method 3051a, and analyzed with graphite furnace atomic absorption spectrophotometry. Arsenic concentrations varied greatly in Gainesville, ranging from 0.21 to approximately 660 mg kg(-1) with a geometric mean (GM) of 0.40 mg kg(-1) (after discarding outliers), which was significantly lower than the GM of 2.81 mg kg(-1) in Miami, although Miami samples ranged only from 0.32 to approximately 110 mg kg(-1). Arsenic concentrations in 29 and 4% of the Gainesville soil samples and 95 and 33% of the Miami samples exceeded the Florida residential and commercial SCTL, respectively. This study is the first to provide information on arsenic distribution in urban soils of Florida, and the data are useful for assessing arsenic contamination and determining the need for remediation.

Arsenic↗

Human health risks from arsenic in soils: does one model fit all?

In the absence of a "soil model" on arsenic bioavailability, many investigators conducting baseline risk assessments of arsenic-enriched sites have assumed that all arsenic present in the soil is bioavailable. This assumption overestimates actual human health risk because various geochemical forms of arsenic are stable, or insoluble, in human digestive juices. The authors conducted a laboratory incubation study to analyze the in vitro bioavailability of arsenic in soils as a function of soil properties. Four different soil types were selected on the basis of their potential differences with respect to arsenic reactivity. Each soil was amended with sodium arsenite at a rate representative of a routine 1-yr application of arsenical pesticide in an agricultural system. The soils were incubated for 1 yr, after which the authors measured soil-specific total and bioavailable arsenic concentrations. Results demonstrated that soil physicochemical properties significantly affect arsenic bioavailability, and hence estimates of cancer risk, which in turn affect site cleanup cost projections.

Agriculture↗

Infrequent p53 mutations in arsenic-related skin lesions.

Oral arsenic exposure increases the risk for a variety of benign and malignant skin lesions, but the molecular mechanism of the carcinogenic effect is poorly understood. Arsenic-related squamous cell carcinomas of the skin can develop either de novo or progress from Bowen's disease lesions. Arsenic-related basal cell carcinomas develop usually in non-sun-exposed areas and are multiple. Because p53 tumor suppressor protein is a protective cellular molecule against environmental carcinogens and mutations in the p53 gene are frequent in nonmelanoma skin cancers, we studied p53 in 23 premalignant or malignant skin lesions from seven patients with a history of arsenic medication. The eighth patient studied (with six lesions) had a long standing exposure to UV radiation. Accumulation of the p53 protein was detected (with a monoclonal DO-7 antibody) in 78% of the lesions from cases with arsenic exposure. Two of the six (30%) arsenic-related premalignant lesions and in addition one UV related carcinoma in situ lesion were clearly and repeatedly positive when p53 exons 5 to 8 were screened by a nonradioactive single-strand conformation polymorphism (SSCP) analysis. Only one of the arsenic-related lesions was confirmed by sequencing to have a mutation (a CC to TT double transition). No indications of mutations were found among the 18 basal cell carcinoma or two squamous cell carcinoma lesions studied. Our results suggest that the frequent accumulation of p53 protein in arsenic-related skin lesions is not due to p53 mutations. which may not be a prerequisite in the development of arsenic-induced skin cancers.

Aged↗

Arsenic-induced NFkappaB transactivation through Erks- and JNKs-dependent pathways in mouse epidermal JB6 cells.

Tumor promoting effects of arsenic are believed to be associated with its transactivation activity on transcription factors, such as AP-1 and NFkappaB. However, the results from different groups studying the effects of arsenic on NFkappaB activation are contradictory in different cell models. Since arsenic is a strong skin carcinogen, we have investigated the activation of NFkappaB by arsenic in a mouse skin epidermal cell line, JB6 cells. Exposure of cells to arsenite or arsenate led to NFkappaB transactivation in mouse epidermal JB6 NFkappaB-luciferase reporter stable transfectants, C141 NFkappaB mass1. This induction of NFkappaB activity by arsenic was dose- and time-dependent. The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1. That Erks activation is required for arsenic-induced NFkappaB transactivation was further supported by the findings that arsenic-induced NFkappaB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.

Animals↗

Porphyrins as early biomarkers for arsenic exposure in animals and humans.

We studied the effect of arsenic exposure on the haem biosynthetic pathway in the rat and humans. Significant increases in protoporphyrin IX, coproporphyrin III, coproporphyrin I were observed in the blood, liver and kidney, and in the urine of rats after a single dose of arsenic. The level of increase was dependent on the arsenic species present. Most of porphyrin concentrations in the tissues increased within 24 hr and urinary excretion elevated within 48 hr. In the human study, we collected urine samples from 113 people who live in Xing Ren of Guizhou Province, a coal-borne arsenicosis endemic area in southwest of PR China and from 30 people who live in Xing Yi (about 80 km southwest of Xing Ren) where arsenicosis is not prevalent. We analyzed the urinary porphyrins using HPLC. Results indicate that all urinary porphyrins were higher in the arsenic exposed group than those in the control group. Women, children and older age people spend much of their time indoors, they had greater increases of urinary arsenic and porphyrins. They were the higher risk groups among the study subjects. A positive correlation between the urinary arsenic levels and porphyrin concentrations demonstrated the effect of arsenic on haem biosynthesis. Significant alteration in the porphyrin excretion profiles of the younger age (<20 y) arsenic exposed group suggested that porphyrins could be used as early warning biomarkers for chronic exposure to arsenic.

Age Factors↗

[Peripheral circulatory disorders and acrocyanosis in arsenic exposed Moselle wine-growers].

Peripheric circulatory disturbances and acrocyanosis in Moselle vinedressers injured by arsenic. During the years 1972--1975 a total number of 100 vine-dressers came for medical treatment because of late injures caused by arsenic intoxication. That is an average of 400 examinations per year 1600 control examinations within four years. These patients belonged to the age-classes 1890--1923, and the average time of exposure to arsenic was 20 years. After years of being exposed to arsenic, and even years after the exposure to it has stopped, there are those so-called late injures caused by arsenic. There are typical arsenic melanisms on the forehad-temple-rim where the hair begins to grow, on the nape of the neck, on the shoulders, chest, arms, and on the back of the hands which pass into precanceroses and carcinomas. The average time until the first late injuries caused by arsenic occur is 26 years. However, there have been latence periods of up to 50 years. This depends mainly on the amount of arsenic absorbed during the time. There are skin alterations which resemble very much an acrodermatitis chronica atrophicans Herxheimer. Histological examinations rather showed the symptoms of an endangiitis obliterans with atrophy of the cutis. These symptoms were found in 60--70% of the 50--60 years old patients, in 80--90% of the 60--70 years old patients, and in 90--95% of the 70--80 years old patients. Simultaneously there are distinct peripheric circulatory disturbances, cyanosis of the lips, dyspnoea, and an emphysema together with typical cardiac insufficiency. Foot and finger pulse are distinctly slower, and the temperature of the skin is remarkably lower. While people grow older the cyanosis gets worse. With a control group of patients who hadn't been exposed to arsenic these symptoms had only been found on 1--2%.

Age Factors↗

Arsenic, cadmium and lead levels in hair and toenail samples in pakistan.

We collected toenail and hair samples from 160 subjects, 83 males and 77 females, residing in Lahore city and its suburban areas in Pakistan, and examined the concentrations of arsenic, cadmium, lead and other metals using inductively coupled plasma mass spectrometry (ICP-MS). The mean hair and toenail arsenic levels were 0.31 ppm and 0.70 ppm, respectively. The correlation coefficient between log-transformed values of hair and toenail arsenic levels was 0.16 (p=0.051). After excluding a subject with hair and toenail arsenic levels as high as 1.12 ppm and 4.72 ppm, respectively, the correlation coefficient was 0.27 (p=0.001). Arsenic levels observed in the present study were relatively higher than in most developed countries. Hair or toenail arsenic concentration was not affected by sex, area of origin, place of residence and education, but toenail arsenic levels increased with age (p=0.029). Fish consumption was inversely related to arsenic levels, suggesting that consumption of beans , which are the main staple of poor people living in the study area who cannot afford to eat fish frequently, may be the source of arsenic exposure among the residents of Lahore and its suburban areas. The mean hair and toenail cadmium levels in the present study were 0.08 ppm and 0.05 ppm, respectively. The correlation coefficient between log-transformed values of hair and toenail cadmium levels was 0.17 (p=0.034). Cadmium levels were lower compared to those reported from developed countries, including Japan. The mean hair and toenail lead levels were 3.53 ppm and 2.11 ppm, respectively. The correlation coefficient between log-transformed values of hair and toenail lead levels was 0.15, which was not statistically significant (p=0.055). When a female subject with toenail lead of 52.4 ppm was excluded, the correlation was 0.17 (p=0.036). Lead levels observed in the present study were similar to those reported from developed countries. In the present study, relatively high lead toenail values were observed among children. The levels of cadmium and lead in hair but not in toenails were higher among those living in central Lahore than among those living outside Lahore, suggesting that dust containing those heavy metals was attached to hair samples due to a typical urban environment with heavy traffic load, congested population and industrial activities.

Adolescent↗

Effect of hexane extract of spirulina in the removal of arsenic from isolated liver tissues of rat.

The present study was conducted to investigate whether the active compound(s) of spirulina is present in its -- alcohol extract, hexane extract, DCM extract or in their residues. In phase I the accumulation of arsenic in isolated liver tissues of rat at different incubation period (15, 30, 45 minutes) was seen. In phase II arsenic-loaded liver tissues were incubated in presence and absence of alcohol extract, alcohol extraction residues, hexane extract, hexane extraction residues, DCM extract and DCM extraction residues of spirulina respectively. The percentage removal of arsenic from liver tissues by different extracts and residues of spirulina was estimated by Atomic Absorption Spectrophotometer. In phase III arsenic-loaded liver tissues were incubated in presence and absence of different concentration of hexane extract of spirulina and the percentage removal of arsenic from liver tissues was estimated. This study showed that the accumulation of arsenic in isolated liver tissue was time dependent and highest accumulation found was 0.69 microg/g tissues after 45 minutes incubation, which was highly significant. The percentage removal of arsenic from arsenic loaded liver tissues by alcohol extract, alcohol extraction residues, hexane extract, hexane extraction residues, DCM extract, DCM extraction residues were 33.8%,4.4%,83.0%,10.2%,7.3% and 2.9%, respectively. The percentage removal of arsenic by hexane extract at the concentration of 1, 10, 100 microg were 13.2%, 29.4% and 89.7%, respectively. Among the different extracts and residues of spirulina the hexane extract causes highly significant (p<0.001) removal. In conclusion the present study suggests that the active compound(s) of spirulina is present mostly in its hexane extract.

Animals↗