Oxidative Stress Level in the Testes of Mice and Rats during Nickel Intoxication (original) (raw)
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Nickel toxicology with reference to male molecular reproductive physiology
Reproductive Biology, 2020
The toxicity of metals is a known phenomenon. Nickel toxicity is very common since nickel is used extensively both industrially and in items of personal use such as utensils and jewellery. Here we discuss human exposure to nickel and its toxicity in the light of the available scientific evidence to understand its underlying pathophysiology. The ability of Ni +2 to get oxidized to Ni +3 renders it's potential of generating reactive oxygen species (ROS) in the system leading to oxidative stress. Carcinogenesis, apoptosis induction, contact dermatitis, epigenetic changes, and alteration in gene regulation are a result of overexposure of nickel. Our focus is on how nickel affects the male reproductive physiology. Nickel primarily drives ROS mediated perturbations in the male reproductive system. It influences zinc metabolism, which is critical for sperm stability and affects the structure of DNA binding proteins, including protamines, thereby affecting sperm function.
α-Tocopherol ameliorates nickel induced testicular oxidative and nitrosative stress in albino rats
Journal of Basic and Clinical Physiology and Pharmacology, 2012
Background: Heavy metals generate free radicals and induce oxidative and nitrosative stress with depletion of antioxidants. In this study, we have evaluated the benefi cial effects of α -tocopherol against nickel sulfate exposed testicular dysfunction. Methods: We studied the effect of supplementation of α -tocopherol (10 mg/100 g body weight, i.m.) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced testicular oxidative and nitrosative stress in Wister strain male albino rats. Serum and testicular nitric oxide, L-ascorbic acid and serum α -tocopherol concentrations were evaluated. We also evaluated sperm count, motility and histopathology of testes. Results: Nickel treated rats showed signifi cantly decreased body weight, testicular somatic index, sperm count, sperm motility, serum and testicular L-ascorbic acid concentration and serum α -tocopherol level as compared to their controls. However, simultaneous treatment with nickel sulfate and α -tocopherol produced a remarkable improvement of all the above parameters when compared with treatment with nickel alone. Nickel treated rats also had signifi cantly increased serum and testicular nitric oxide concentrations as compared to their controls. However, simultaneous treatment with nickel sulfate and α -tocopherol signifi cantly decreased nitric oxide concentrations in both serum and testes, respectively, as compared to nickel treatment alone. Histopathology of the testes revealed tortuous seminiferous tubules, loss of spermatogenesis process ( > 75 % ), congestion and necrosis in nickel sulfate treated rats, whereas rats simultaneously treated with nickel sulfate and α -tocopherol had almost normal seminiferous tubules and near normal spermatogenesis as compared to nickel alone treated rats.
Medycyna Weterynaryjna, 2019
Nickel is a ubiquitous environmental heavy metal pollutant. It is also known to be the fifth most common element in the world (20). Owing to its unique physical and chemical properties, metallic nickel and its compounds have a wide range of use in modern industries (15). Nickel can be obtained by metallurgical activities, including mining, refining, electroplating, welding, and the manufacture of stainless steel (7, 15). Nickel is also a major component of alloys found in orthopaedic plate and screw assemblies and is used in the manufacture of artificial organs (12). Research results suggest that nickel could be an essential trace metal that enhances growth in birds and mammals at very low doses (ppb) (14). However, high doses of nickel may show a carcinogenic effect in both humans and animals (14). The exposure of humans and animals to nickel may occur by ingestion, dermal contact, and inhalation (10). Although nickel uptake occurs mostly via food and water consumption, in occupational settings the primary route of nickel-induced toxicity is inhalation (17). In the body, nickel mainly accumulates in the kidneys, lungs, liver and testes and causes tissue damage (10, 20), resulting in neurotoxicity, nephrotoxicity, hepatotoxicity, reproductive toxicity, genotoxicity, as well as an increased risk of cancer (10). The reproductive system is known to be more sensitive to hazardous factors such as nickel and other metals that pollute the environment (7, 32). Animal research has demonstrated nickel-induced adverse effects on the structure and functions of the testes, seminal vesicles, and prostate gland, as well as on spermatozoa (14). Moreover, research has shown that nickel causes damage to the testicular structure in experimental animals, which is manifested by an increased percentage of abnormal spermatozoa, fragmentation of DNA strands, cell damage, necrosis, cell apoptosis, oxidative stress and the generation of reactive oxygen species (ROS) (32). The toxic and carcinogenic effects of nickel compounds have been well demonstrated in humans and experimental animals, yet the underlying mechanisms of nickel-induced reproductive toxic effects in males remain unclear (6). Animal experiments have demonstrated the occurrence of testicular toxicity and oxidative stress after exposure to high doses of nickel. In
Journal of Basic and Clinical Physiology and Pharmacology, 2007
We studied the effect of oral supplementation with L-ascorbic acid (50 mg/ 100g body weight) on nickel sulfate 2.0 mg/100g body weight, i.p.) induced lipid peroxidation in the testes of Wister strain male albino rats. Testicular lipid peroxide and glutathione (GSH) levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated. Nickel sulfate treatment significantly increased the level of testicular lipid peroxide and decreased all antioxidant enzymes activities and GSH concentration. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on testicular lipid peroxide and GSH concentration as well as antioxidant enzymatic defense system.
Combined effects of cadmium and nickel on testicular xenobiotic metabolizing enzymes in rats
Biological Trace Element Research, 2002
When male rats were given a single dose of cadmium (Cd) (3.58 mg CdCl2·H2O/kg, ip) 72 hr prior to sacrifice, the testicular 7-ethoxyresorufin O-deethylase (EROD) and glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), 1,2-epoxy-3-(p-nitrophenoxy)-propane (EPNP), and cumene hydroperoxide (CHPx) decreased significantly as compared to controls. Cd also inhibited reduced glutathione (GSH) level while increasing the lipid peroxidation (LP) level significantly. When the animals were given a single dose of nickel (Ni) (59.5 mg NiCl2·6H2O/kg, ip) 16 hr prior to sacrifice, significant decreases were observed in EROD and GST activities toward CDNB, EAA, EPNP, and CHPx, and GSH level. No significant alterations were noted in DCNB GST activity and LP level by Ni. For the combined treatment, rats received the single dose of Ni 56 hr after the single dose of Cd and were killed 16 hr later. In these animals, lesser depressions were observed on EROD activity and LP level than those of Cd alone. The combination of metals significantly inhibited GST activities and GSH level but not to a greater degree than noted by Cd or Ni alone. Plasma testosterone levels of Cd-, Ni-, and combination-treated rats decreased significantly compared to controls. The strongest depression was achieved by Cd alone. Cd, both alone and in combination with Ni, increased the tissue Ni uptake significantly. Ni, however, did not produce such an effect on the tissue uptake of Cd in either case. Cd treatment caused interstitial edema and coagulation necrosis in seminiferous tubules and also caused fibrinoidal necrosis in vascular endothelium. Ni treatment did not produce any pathological testicular alterations compared to controls. Combined treatment produced fewer pathological alterations (i.e., only interstitial edema) than that of Cd treatment. These results reveal that the combination of Cd and Ni does not have a synergistic effect on testicular xenobiotic metabolizing enzymes, and in contrast, Ni has an ameliorating effect on pathological disturbances caused by Cd alone in the rat testis.
Nickel, its adverse health effects & oxidative stress
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 sulphhydryl homeostasis. The primary route for nickel toxicity is depletion of glutathione and bonding to sulphhydryl 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.
Objective: This study investigates the effects of troxerutin on nickel (Ni)-induced oxidative stress in rats. Methods: Nickel as nickel sulfate (20 mg/kg body weight (b.w.)) was administered intraperitoneally for 20 days to induce toxicity in the subject rats. The levels of stress markers AST, ALT, ALP, LDH, and GGT in the hepatic tissue were significantly increased while a decrease in the levels of enzymic and non-enzymic antioxidants was observed in Ni intoxicated rats. Results: Oral administration of troxerutin along with Ni for 20 days in a dose-dependent manner significantly reverted the stress markers in the liver tissue to near normal level. Troxerutin exhibited significant protection at 100 mg/kg b.w. Histopathological studies also supported the above findings. Conclusions: Thus, we conclude that troxerutin preserved the histo-architecture and ameliorated stress markers in the liver tissue of Ni-intoxicated rats.
ARID International Journal for Science and Technology (AIJST, 2022
Semen samples were collected from healthy people (control group for comparison), asthenospermia infertility patients, and unexplained infertility patients from male donors who attended the Fertility Center at Al-Sadr Teaching Hospital in Al-Najaf Al-Ashraf / Iraq for the period from 1/12/2020 to 25/3 /2021. The present study aims to estimate the concentration of manganese, nickel, and aluminum in semen as one of the factors that cause oxidative stress in male infertility. The atomic absorption spectrometry was used to estimate the concentrations of the elements and the statistical analysis by the Tukey One Way method in the Graph Pad Prism program to determine the relationships between the study elements and the parameters of semen in men. The results of the study showed a significant increase (P < 0.05) in the level of nickel and aluminum concentrations (490 ± 27.57 and 450.3 ± 17.92 μg/L, respectively) and a significant decrease (P < 0.05) in the concentration of manganese (202 ± 8.718 ppm). ) in the semen group of men with asthenospermia in comparison with the healthy fertile group (as a control group) (161.7 ± 5.963, 307.5 ± 10.58 μg/L and 309.2 ± 1.470 ppm), respectively. The results also revealed the existence of many negative relationships between the concentration of elements and semen parameters and between the same concentrations. The study concluded that the concentrations of these elements are a factor of stress oxidants that appear in cases of asthenozoospermia or may not change in other types of infertility and remain unexplained infertility.
Reproductive toxicology of nickel – Review
Journal of Environmental Science and Health, Part A, 2012
The goal of this minireview is to summarize our current knowledge on the reproductive toxicity of soluble nickel salts. We made an attempt to present the most relevant data obtained from in vivo and in vitro experiments performed on mammals, mammalian primary cell cultures and cell lines. Nickel has been demonstrated to disturb the mammalian reproductive functions at several levels of regulation. The results of previous investigations indicate that the hormonal effects may play an important role in the reproductive toxicology of nickel both at the neuroendocrine and gonadal levels in the hypothalamic-pituitary-gonadal (HPG) axis. At the molecular level, it may be important that nickel may substitute certain other metals in metal dependent enzymes, leading to an altered protein function. It readily crosses the cell membrane via calcium channels and competes with calcium for specific receptors. Nickel can cross-link aminoacids to DNA, lead to formation of reactive oxygen species (ROS), moreover mimic hypoxia. These changes may lead to the activation of some signaling pathways, subsequent transcription factors and eventually to alterations in gene expression and cellular metabolism. These events are likely to be involved in the reproductive toxicity of nickel.