Effect of nickel on testicular nucleic acid concentrations of rats on protein restriction
TL;DR: The results indicate that nickel influences the expression of genetic information by reducing testicular nucleic acids and protein concentration in both dietary experimental groups of animals.
Abstract: The nucleic acids (DNA and RNA) and total protein concentration in testes were estimated in male Wistar strain rats treated intraperitorally with nickel sulfate (2.0 mg/100 g body weight) on alternate days for 10 dosages. In both normal (18% casein) and protein-restricted (5% casein) experimental animals, the nucleic acids and total protein concentration were found to decrease significantly compared to the corresponding controls. Sperm count and sperm motility were also reduced in both experimental groups of animals. The results indicate that nickel influences the expression of genetic information by reducing testicular nucleic acids and protein concentration in both dietary experimental groups.
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TL;DR: A selective review on nickel and effect of its acute, subchronic and chronic doses on certain metabolically active tissues in human as well as animals is presented.
Abstract: Nickel-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen species is reviewed. Nickel is a known haematotoxic, immunotoxic, neurotoxic, genotoxic, reproductive toxic, pulmonary toxic, nephrotoxic , hepatotoxic and carcinogenic agent. This article presents a selective review on nickel and effect of its acute, subchronic and chronic doses on certain metabolically active tissues in human as well as animals. Nickel exposure causes formation of free radicals in various tissues in both human and animals which lead to various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulphydryl homeostasis. The primary route for nickel toxicity is depletion of glutathione and bonding to sulphydryl groups of proteins. Nickel homeostasis, nickel-induced activation of signaling pathways and the protective role of enzymatic and non-enzymatic antioxidants against nickel toxicity and carcinogenicity are also discussed.
477 citations
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
TL;DR: The findings suggest that testicular toxicity of nickel compounds may be related to enhanced production of reactive oxygen species, probably mediated through oxidative damage to macromolecules, including damage to DNA.
Abstract: Oxidative stress (OS) mechanisms are speculated to play a significant role in nickel-induced toxic effects and their carcinogenic potency. Although nickel-induced oxidative damage in somatic tissues is well demonstrated, evidence of the involvement of a similar mechanism(s) in nickel-induced testicular dysfunction and associated genotoxic effects is scarce. Hence, the present study aimed to investigate the nickel-induced OS response in testis and the associated genotoxic implications in vivo. Initially, the toxicity profile of nickel chloride was determined in adult albino mice (CFT-Swiss) following administration (intraperitoneal) of single doses. Subsequently, multiple sublethal doses (1.25, 2.5, and 5.0 micromol/100 g of body weight per day for 3 days) were used to characterize effects on testicular histoarchitecture, lipid peroxidation (LPO) in testis (homogenates, microsomal or mitochondrial fractions) and epididymal sperm, DNA damage, induction of apoptosis in testis, and incidence of sperm head abnormalities. Although short-term doses of nickel induced only a minimal LPO response, multiple doses elicited a moderate (15% to 30%) increase in LPO in whole homogenates and higher dose-related increases in both mitochondrial (20% to 50%) and microsomal fractions (25% to 60%). This was associated with a significant increase in DNA damage in the testis as evidenced by increased single-strand breaks (fluorimetric analysis of DNA unwinding assay). Further, at higher doses, nickel-induced apoptosis was demonstrable in the testis biochemically. Although caudal sperm counts determined at all sampling weeks showed no alterations, analysis for head abnormalities revealed a nearly 3- to 4-fold increase in the percentage of abnormal sperms among the nickel-treated males during the first 3 weeks. Furthermore, mating of nickel-treated (2.5 micromol/100 g of body weight per day for 5 days) males sequentially for a period of 5 weeks with untreated females resulted in a significant increase in male-mediated dominant lethal-type mutations (the frequency of dead implantations) during the first 3 weeks, suggesting a stage-specific effect on postmeiotic germ cells. These findings suggest that testicular toxicity of nickel compounds may be related to enhanced production of reactive oxygen species, probably mediated through oxidative damage to macromolecules, including damage to DNA.
168 citations
TL;DR: This review summarizes the effects of more than 20 metals that, research has indicated, may influence male reproductive health and suggests a need for further research in those chemicals that are reactive and capable of covalent interactions in biological systems.
Abstract: This review summarizes the effects of more than 20 metals that, research has indicated, may influence male reproductive health. Though males lack an apparent, easily measurable reproductive cycle, progress has been made in evaluating tests to identify chemical hazards and estimate reproductive health risks. Some agents discussed in this review are well known to have potential toxic effects on the male reproductive system, whereas some are not so well established in toxicology. This review attempts to cover most of the known toxicants and their effects on male fertility. The literature suggests a need for further research in those chemicals that are reactive and capable of covalent interactions in biological systems, as well as those defined as mutagens and/or carcinogens, to cause aneuploidy or other chromosomal aberrations, affect sperm motility in vitro, share hormonal activity or affect hormone action, and those that act directly or indirectly to affect the hypothalamo-pituitary-gonadal axis.
116 citations
Cites background from "Effect of nickel on testicular nucl..."
...Reports suggested nickel exposure causes decrease in weights of testicular and accessory sex organs and decrease in testicular steroidogenic enzymes activities (Δ(5) 3β-HSD and 17β-HSD) (Das and Dasgupta, 2000)....
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...Reports suggested nickel exposure causes decrease in weights of testicular and accessory sex organs and decrease in testicular steroidogenic enzymes activities (Δ5 3β-HSD and 17β-HSD) (Das and Dasgupta, 2000)....
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...Effects of nickel compounds on reproduction in rodent models are well documented (Pandey et al., 1999; Das and Dasgupta, 2000)....
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...…fertility in mice (Doreswamy et al., 2004), decreased DNA, RNA, and total protein in testes, and decreased sperm count and motility in rats (Das and Dasgupta, 2000), and decreased absolute and relative weights of testes, epididymides, seminal vesicles and prostate gland, decreased sperm…...
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..., 2004), decreased DNA, RNA, and total protein in testes, and decreased sperm count and motility in rats (Das and Dasgupta, 2000), and decreased absolute and relative weights of testes, epididymides, seminal vesicles and prostate gland, decreased sperm count and motility, and increased abnormal sperm morphology in mice (Pandey et al....
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TL;DR: Understanding the mechanism of Ni-induced apoptosis may help in designing measures to prevent Ni toxicity, and participation by reactive oxygen species, mitochondria, endoplasmic reticulum, Fas, and c-Myc participate in Ni- induced cell apoptosis.
Abstract: High concentrations of nickel (Ni) are harmful to humans and animals. Ni targets a number of organs and produces multiple toxic effects. Apoptosis is important in Ni-induced toxicity of the kidneys, liver, nerves, and immune system. Apoptotic pathways mediated by reactive oxygen species (ROS), mitochondria, endoplasmic reticulum (ER), Fas, and c-Myc participate in Ni-induced cell apoptosis. However, the exact mechanism of apoptosis caused by Ni is still unclear. Understanding the mechanism of Ni-induced apoptosis may help in designing measures to prevent Ni toxicity.
103 citations
References
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TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
289,852 citations
21,056 citations
TL;DR: The present study arose from the observation that a more intense colour was sometimes produced if, instead of being heated at 1000 for 10 min., the reaction mixture was allowed to stand overnight at room temperature.
Abstract: Of the colour reactions available for the determination and identification of deoxyribonucleic acid (DNA), the reaction with diphenylamine in a mixture of acetic and sulphuric acids at 1000 (Dische, 1930) has been perhaps the most widely used. The present study arose from the observation that a more intense colour was sometimes produced if, instead of being heated at 1000 for 10 min., the reaction mixture was allowed to stand overnight at room temperature. As a result of this observation the procedure has been modified, principally by adding acetaldehyde to the reagents and by allowing the solution to stand for about 17 hr. at 30° instead of heating it at 1000. The modified method is 3-5 times as sensitive as Dische's original procedure, and several substances which interfere in the original method do not do so in the modified procedure. Some observations on the mechanism of the reaction have been made; in particular it was discovered that there is a liberation of inorganic orthophosphate from DNA during the early stages of the reaction. This finding has a bearing on the structure of DNA. The modified method has already been used in an investigation of nucleic acid metabolism during bacteriophage multiplication (Burton, 1955).
13,649 citations
Book•
01 Jan 1977
TL;DR: This book discusses the history of zinc, its application in agriculture, and its applications in the management of soil-Plant-Animal relations.
Abstract: Zinc, KM Hambidge Iodine, BS Hetzel and GF Maberly Selenium, OA Levander Lead, J Quarterman Cadium, K Kostial Arsenic, M Anke Silicon, EM Carlisle Lithium, W Mertz Aluminum, AC Alfrey Other Elements, FH Nielsen Soil-Plant-Animal Relationships, WH Allaway Each chapter includes references Index
4,557 citations