Modifying role of Phyllanthus emblica and ascorbic acid against nickel clastogenicity in mice.
TL;DR: Aqueous extract of edible dried fruits of Phyllanthus emblica was fed to Mus musculus for seven consecutive days prior to treatment with different doses of nickel chloride, finding the greater efficacy of the fruit extract could be due to the interaction of its various natural components rather than to any single constituent.
About: This article is published in Cancer Letters.The article was published on 1991-07-26. It has received 59 citations till now. The article focuses on the topics: Dried fruit & Ascorbic acid.
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TL;DR: A review for the first time summarizes the results related to these properties and also emphasizes the aspects that warrant future research to establish its activity and utility as a cancer preventive and therapeutic drug in humans.
Abstract: Emblica officinalis Gaertn. or Phyllanthus emblica Linn, commonly known as Indian gooseberry or amla, is arguably the most important medicinal plant in the Indian traditional system of medicine, the Ayurveda. Various parts of the plant are used to treat a range of diseases, but the most important is the fruit. The fruit is used either alone or in combination with other plants to treat many ailments such as common cold and fever; as a diuretic, laxative, liver tonic, refrigerant, stomachic, restorative, alterative, antipyretic, anti-inflammatory, hair tonic; to prevent peptic ulcer and dyspepsia, and as a digestive. Preclinical studies have shown that amla possesses antipyretic, analgesic, antitussive, antiatherogenic, adaptogenic, cardioprotective, gastroprotective, antianemia, antihypercholesterolemia, wound healing, antidiarrheal, antiatherosclerotic, hepatoprotective, nephroprotective, and neuroprotective properties. In addition, experimental studies have shown that amla and some of its phytochemicals such as gallic acid, ellagic acid, pyrogallol, some norsesquiterpenoids, corilagin, geraniin, elaeocarpusin, and prodelphinidins B1 and B2 also possess antineoplastic effects. Amla is also reported to possess radiomodulatory, chemomodulatory, chemopreventive effects, free radical scavenging, antioxidant, anti-inflammatory, antimutagenic and immunomodulatory activities, properties that are efficacious in the treatment and prevention of cancer. This review for the first time summarizes the results related to these properties and also emphasizes the aspects that warrant future research to establish its activity and utility as a cancer preventive and therapeutic drug in humans.
185 citations
Cites background from "Modifying role of Phyllanthus embli..."
..., 1990), nickel (Dhir et al., 1991), cesium chloride (Ghosh et al....
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...…animals have shown that amla prevents cadmium (Khandelwal et al., 2002), lead (Dhir et al., 1990), aluminium (Dhir et al., 1990), nickel (Dhir et al., 1991), cesium chloride (Ghosh et al., 1992), arsenic (Biswas et al., 1999), chromium (Sai Ram et al., 2003), 3,4-benzo(a)pyrene (Nandi…...
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TL;DR: This review specifically highlighted nickel-induced oxidative stress and possible cell signaling mechanisms as well as addressing the acute, subchronic and chronic nickel toxicities in both human and experimental animals.
Abstract: Toxic metals, including excessive levels of essential metals tend to change biological structures and systems into either reversible or irreversible conformations, leading to the derangement of organ functions or ultimate death. Nickel, a known heavy metal is found at very low levels in the environment. Nickel is available in all soil types and meteorites and also erupts from volcanic emissions. In the environment, nickel is principally bound with oxygen or sulfur and forms oxides or sulfides in earth crust. The vast industrial use of nickel during its production, recycling and disposal has led to widespread environmental pollution. Nickel is discharged into the atmosphere either by nickel mining or by various industrial processes, such as power plants or incinerators, rubber and plastic industries, nickel-cadmium battery industries and electroplating industries. The extensive use of nickel in various industries or its occupational exposure is definitely a matter of serious impact on human health. Heavy metals like nickel can produce free radicals from diatomic molecule through the double step process and generate superoxide anion. Further, these superoxide anions come together with protons and facilitate dismutation to form hydrogen peroxide, which is the most important reason behind the nickel-induced pathophysiological changes in living systems. In this review, we address the acute, subchronic and chronic nickel toxicities in both human and experimental animals. We have also discussed nickel-induced genotoxicity, carcinogenicity, immunotoxicity and toxicity in various other metabolically active tissues. This review specifically highlighted nickel-induced oxidative stress and possible cell signaling mechanisms as well.
170 citations
01 Jan 2015
TL;DR: Overall, the CONTAM Panel concluded that, at the current levels of acute dietary exposure to Ni, there is a concern that Nisensitized individuals may develop eczematous flare-up skin reactions.
Abstract: Opinion on the risks to public health related to the presence of nickel in food and drinking water DTU Orbit (09/12/2018) EFSA CONTAM Panel (EFSA Panel on Contaminants in the Food Chain), 2015. Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water EFSA received a request from the Hellenic Food Authority (EFET) for a scientific opinion on the risk to human health from the presence of nickel (Ni) in food, particularly in vegetables. The EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) decided to extend the risk assessment also to drinking water. The reproductive and developmental toxicity in experimental animals was selected as the critical effect for the assessment of chronic effects of Ni. A tolerable daily intake of 2.8 μg Ni/kg body weight (b.w.) per day was derived from a lower 95 % confidence limit for a benchmark dose at 10 % extra risk (BMDL10) of 0.28 mg/kg b.w. for post-implantation fetal loss in rats. The current dietary exposure to Ni raises concern when considering the mean and 95th percentile chronic exposure levels for all different age groups. The systemic contact dermatitis (SCD) elicited in Ni-sensitive humans after oral exposure to Ni was selected as the critical effect suitable for the assessment of acute effects of Ni. A lowest BMDL10 of 1.1 μg Ni/kg b.w. was derived for the incidence of SCD following oral exposure to Ni of human volunteers. The CONTAM Panel applied a margin of exposure (MOE) approach and considered an MOE of 10 to be indicative of a low health concern. The MOEs calculated considering the estimated mean and the 95th percentile acute exposure levels were considerably below 10 for all age groups. Overall, the CONTAM Panel concluded that, at the current levels of acute dietary exposure to Ni, there is a concern that Nisensitized individuals may develop eczematous flare-up skin reactions. The CONTAM Panel noted the need for mechanistic studies to assess the human relevance of the effects on reproduction and development observed in experimental animals and for additional studies on human absorption of nickel from food, for example in combination with duplicate diet studies.
138 citations
01 Jul 2019
TL;DR: In this paper, a review of both human and environmental nickel toxicity data is presented, which is unique in its covering of both anthropometric and environmental toxicity data, as well as the influence of abiotic factors on the bioavailability and toxicity of Ni2+ ion in different habitats.
Abstract: Nickel (Ni) metal and Ni compounds are widely used in applications like stainless steel, alloys, and batteries. Nickel is a naturally occurring element in water, soil, air, and living organisms, and is essential to microorganisms and plants. Thus, human and environmental nickel exposures are ubiquitous. Production and use of nickel and its compounds can, however, result in additional exposures to humans and the environment. Notable human health toxicity effects identified from human and/or animal studies include respiratory cancer, non-cancer toxicity effects following inhalation, dermatitis, and reproductive effects. These effects have thresholds, with indirect genotoxic and epigenetic events underlying the threshold mode of action for nickel carcinogenicity. Differences in human toxicity potencies/potentials of different nickel chemical forms are correlated with the bioavailability of the Ni2+ ion at target sites. Likewise, Ni2+ has been demonstrated to be the toxic chemical species in the environment, and models have been developed that account for the influence of abiotic factors on the bioavailability and toxicity of Ni2+ in different habitats. Emerging issues regarding the toxicity of nickel nanoforms and metal mixtures are briefly discussed. This review is unique in its covering of both human and environmental nickel toxicity data.
114 citations
TL;DR: It is suggested that chronic occupational exposure to Cr and Ni during welding could lead to increased levels of DNA damage, which could affect human health risk from exposure.
Abstract: Chromium (Cr) and nickel (Ni) are widely used industrial chemicals. Welders in India are inclined to possible occupational Cr and Ni exposure. The carcinogenic potential of metals is a major issue in defining human health risk from exposure. Hence, in the present investigation, 102 welders and an equal number of control subjects were monitored for DNA damage in blood leucocytes utilizing the Comet assay. The two groups had similar mean ages and smoking prevalences. A few subjects were randomly selected for estimation of Cr and Ni content in whole blood by inductively coupled plasma mass spectrometry. The Comet assay was carried out to quantify basal DNA damage. The mean comet tail length was used to measure DNA damage. Welders had higher Cr and Ni content when compared with controls (Cr, 151.65 versus 17.86 micro g/l; Ni 132.39 versus 16.91 micro g/l; P < 0.001). The results indicated that the welders had a larger mean comet tail length than that of the controls (mean +/- SD, 23.05 +/- 3.86 versus 8.94 +/- 3.16; P < 0.001). In addition, the micronucleus test on buccal epithelial cells was carried out in a few randomly selected subjects. Welders showed a significant increase in micronucleated cells compared with controls (1.30 versus 0.32; P < 0.001). Analysis of variance revealed that occupational exposure (P < 0.05) had a significant effect on DNA mean tail length, whereas smoking and age had no significant effect on DNA damage. The current study suggested that chronic occupational exposure to Cr and Ni during welding could lead to increased levels of DNA damage.
109 citations
Cites background from "Modifying role of Phyllanthus embli..."
...The genotoxic effects of Ni and Ni compounds have been demonstrated in various short-term in vitro (Hong et al., 1997; Lei et al., 2001; Blasiak et al., 2002) and in vivo (Dhir et al., 1991; Saplokoglu et al., 1997) tests....
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References
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TL;DR: Dietary intake of natural antioxidants could be an important aspect of the body's defense mechanism against these agents of cancer and other age-related diseases.
Abstract: The human diet contains a great variety of natural mutagens and carcinogens, as well as many natural antimutagens and anticarcinogens. Many of these mutagens and carcinogens may act through the generation of oxygen radicals. Oxygen radicals may also play a major role as endogenous initiators of degenerative processes, such as DNA damage and mutation (and promotion), that may be related to cancer, heart disease, and aging. Dietary intake of natural antioxidants could be an important aspect of the body’s defense mechanism against these agents. Many antioxidants are being identified as anticarcinogens. Characterizing and optimizing such defense systems may be an important part of a strategy of minimizing cancer and other age-related diseases.
2,924 citations
01 Jan 1976
TL;DR: Micronuclei originate from chromatin which for different reasons has been lagging in anaphase, and in the course of telophase this material is included into one or the other daughter cell where it either can fuse with the main nucleus or form one or several secondary nuclei.
Abstract: Micronuclei originate from chromatin which for different reasons has been lagging in anaphase (Fig. la-d). In the course of telophase this material is included into one or the other daughter cell where it either can fuse with the main nucleus or form one or several secondary nuclei. These are, as a rule, considerably smaller than the principal nucleus and are therefore called micronuclei. Lagging has two main causes: chromosome breakage and malfunction of the spindle apparatus. In the first case the lagging elements are acentric chromosome fragments and di- or multicentrics connected by bridges, and in the second case they consist of entire chromosomes.
629 citations
479 citations
352 citations
TL;DR: In this chapter, inhibitors of mutagenesis and carcinogenesis that can arise as components of diet have been reviewed and most of the inhibitors have been demonstrated to be effective against a specific class of mutagens or carcinogens.
Abstract: Dietary inhibitors of mutagenesis and carcinogenesis are of particular interest because they may be useful for human cancer prevention. Several mutagenesis inhibitors have been demonstrated to be carcinogenesis inhibitors also, e.g., ellagic acid, palmitoleic acid, and N-acetylcysteine. This means that the search for mutagenesis inhibitors may be useful for discovering anticarcinogenic agents. Many mutagenesis inhibitors have been discovered by the use of short-term assays, particularly the Ames Salmonella test. This simple in vitro system has provided opportunities to elucidate the mechanisms of inhibition. The elucidation of the mechanism may allow us to infer the possible anticarcinogenic activity of the reagent. In this chapter, inhibitors of mutagenesis and carcinogenesis that can arise as components of diet have been reviewed. Most of the inhibitors have been demonstrated to be effective against a specific class of mutagens or carcinogens. Therefore, it may be argued that these inhibitors are antagonistic only to those particular agents. Here again, understanding of the mechanisms of these inhibitions is necessary for the assessment. Dietary inhibitors reviewed in this article include: (1) as inhibitors of mutagenesis: porphyllins, fatty acids, vitamins, polyphenols, and sulfhydryl compounds, (2) as inhibitors of carcinogenesis: vitamins A, E and C, ellagic acid, sulfhydryl compounds, fats, selenium, calcium, and fiber. Further studies in this area of science appear to help establish the recipe of a healthy diet.
310 citations