ABSTRACT
As lithium (Li) stands out as a crucial component of batteries, the inappropriate disposal of electronic gadgets might drive Li pollution in environmentally sensitive environments, such as dumps, where castor bean (Ricinus communis) plant communities are usually found. The exposure to high Li concentration is potentially harmful to the environment and humans. Therefore, it is opportune to evaluate the potential of bioindicator species to monitor Li contamination. In this scenario, the present study assessed the effects of Li exposure on the development of castor bean plants exposed to lithium chloride at five Li dosages (0, 5, 10, 20, and 30 mg dm-3). Significant symptoms of phytotoxicity were observed at all doses. Li dosage exhibited increasing impairment effects on plant biometrics, such as stem diameter and the number of leaves, as well as on the SPAD index, nutritional balance, and biomass production. Our findings suggest castor bean as a potential model species for biomonitoring Li-contaminated areas.
Subject(s)
Lithium , Ricinus communis , Ricinus communis/drug effects , Lithium/toxicity , Environmental Monitoring/methods , Ricinus/drug effects , Soil Pollutants/toxicityABSTRACT
Lithium is a key medication for the treatment of psychiatric disorders and is also used in various industrial applications (including battery production and recycling). Here, we review published data on the endocrine-disrupting potential of lithium, with a particular focus on the thyroid hormone system. To this end, we used PubMed and Scopus databases to search for, select and review primary research addressing human and animal health endpoints during or after lithium exposure at non-teratogenic doses. Given the key role of thyroid hormones in neurodevelopmental processes, we focused at studies of the neural effects of developmental exposure to lithium in humans and animals. Our results show that lithium meets the World Health Organization's definition of a thyroid hormone system disruptor - particularly when used at therapeutic doses. When combined with knowledge of adverse outcome pathways linking molecular initiating events targeting thyroid function and neurodevelopmental outcomes, the neurodevelopmental data reported in animal experiments prompt us to suggest that lithium influences neurodevelopment. However, we cannot rule out the involvement of additional modes of action (i.e. unrelated to the thyroid hormone system) in the described neural effects. Given the increasing use of lithium salts in new technologies, attention must be paid to this emerging pollutant - particularly with regard to its potential effects at environmental doses on the thyroid hormone system and potential consequences on the developing nervous system.
Subject(s)
Endocrine Disruptors , Lithium , Thyroid Hormones , Humans , Endocrine Disruptors/toxicity , Animals , Lithium/toxicity , Thyroid Hormones/metabolism , Lithium Compounds , Environmental Pollutants/toxicityABSTRACT
Epilepsy is known to cause alterations in neural networks. However, many details of these changes remain poorly understood. The objective of this study was to investigate changes in the properties of hippocampal CA1 pyramidal neurons and their synaptic inputs in a rat lithium-pilocarpine model of epilepsy. In the chronic phase of the model, we found a marked loss of pyramidal neurons in the CA1 area. However, the membrane properties of the neurons remained essentially unaltered. The results of the electrophysiological and morphological studies indicate that the direct pathway from the entorhinal cortex to CA1 neurons is reinforced in epileptic animals, whereas the inputs to them from CA3 are either unaltered or even diminished. In particular, the dendritic spine density in the str. lacunosum moleculare, where the direct pathway from the entorhinal cortex terminates, was found to be 2.5 times higher in epileptic rats than in control rats. Furthermore, the summation of responses upon stimulation of the temporoammonic pathway was enhanced by approximately twofold in epileptic rats. This enhancement is believed to be a significant contributing factor to the heightened epileptic activity observed in the entorhinal cortex of epileptic rats using an ex vivo 4-aminopyridine model.
Subject(s)
CA1 Region, Hippocampal , Disease Models, Animal , Epilepsy , Lithium , Pilocarpine , Pyramidal Cells , Animals , Pyramidal Cells/pathology , Pyramidal Cells/metabolism , Rats , Epilepsy/chemically induced , Epilepsy/pathology , Epilepsy/physiopathology , Male , CA1 Region, Hippocampal/pathology , Lithium/toxicity , Lithium/pharmacology , Entorhinal Cortex/pathology , Rats, WistarABSTRACT
Spent lithium-ion batteries (LIBs) have emerged as a major source of waste due to their low recovery rate. The physical disposal of spent LIBs can lead to the leaching of their contents into the surrounding environment. While it is widely agreed that hazardous substances such as nickel and cobalt in the leachate can pose a threat to the environment and human health, the overall composition and toxicity of LIB leachate remain unclear. In this study, a chemical analysis of leachate from spent LIBs was conducted to identify its primary constituents. The ecotoxicological parameters of the model organism, rotifer Brachionus asplanchnoidis, were assessed to elucidate the toxicity of the LIB leachate. Subsequent experiments elucidated the impacts of the LIB leachate and its representative components on the malondialdehyde (MDA) level, antioxidant capacity, and enzyme activity of B. asplanchnoidis. The results indicate that both the LIB leachate and its components are harmful to individual rotifers due to the adverse effects of stress-induced disturbances in biochemical indicators, posing a threat to population development. The intensified poisoning phenomenon under combined stress suggests the presence of complex synergistic effects among the components of LIB leachate. Due to the likely environmental and biological hazards, LIBs should be strictly managed after disposal. Additionally, more economical and eco-friendly recycling and treatment technologies need to be developed and commercialized.
Subject(s)
Lithium , Malondialdehyde , Oxidative Stress , Rotifera , Water Pollutants, Chemical , Animals , Rotifera/drug effects , Lithium/toxicity , Malondialdehyde/metabolism , Oxidative Stress/drug effects , Water Pollutants, Chemical/toxicity , Electric Power Supplies , Antioxidants/metabolismABSTRACT
Driven by the global popularity of electric vehicles and the shortage of critical raw materials for batteries, the spent lithium-ion power battery (LIPB) recycling industry has exhibited explosive growth in both quantity and scale. However, relatively little information is known about the environmental risks posed by LIPB recycling, in particular with regards to perfluoroalkyl and polyfluoroalkyl substances (PFAS). In this work, suspect screening and nontarget analysis were carried out to characterize PFAS in soil, dust, water and sediment from a LIPB recycling area. Twenty-five PFAS from nine classes were identified at confidence level 3 or above, including 13 legacy and 12 emerging PFAS, as well as two ultrashort-chain PFAS. Based on the target analysis of 16 PFAS, at least nine were detected in each environmental sample, indicating their widespread presence in a LIPB recycling area. Perfluorodecanoic acid, perfluorooctanesulfonic acid and trifluoromethanesulfonamide showed significant differences in the four phenotypic parameters (growth, movement, survival and fecundity) of Caenorhabditis elegans and were the most toxic substances in all target PFAS at an exposure concentration of 200 µM. Our project provides first-hand information on the existence and environmental risk of PFAS, facilitating the formulation of regulations and green development of the LIPB recycling industry.
Subject(s)
Lithium , Lithium/toxicity , Recycling , Fluorocarbons/toxicity , Electric Power Supplies , Environmental Monitoring , AnimalsABSTRACT
OBJECTIVE: This study aimed to evaluate the protective effects of astaxanthin against lithium-induced nephrotoxicity, focusing on histopathological changes, oxidative stress modulation, and alteration in the expression of key proteins related to apoptosis and inflammation. METHODS: In this study, 56 male rats were utilized and divided into experimental groups subjected to lithium-induced nephrotoxicity, with and without astaxanthin treatment, over 14 and 28 days. The parameters assessed included oxidative stress markers (MDA, GSH, SOD), protein expression levels of BCL-2, BAX, TNF- α, PI3K, NF-κ B-p65, IL-1ß, and comprehensive histopathological examinations to evaluate the integrity of renal tissue. RESULTS: Lithium exposure led to significant renal damage, as evidenced by histological distortions in renal architecture, increased oxidative stress indicated by elevated MDA levels, and dysregulated expressions of apoptotic and inflammatory proteins. Notably, histopathological analysis revealed glomerular and tubular degeneration in lithium-treated groups. Astaxanthin treatment effectively mitigated these effects, demonstrating its efficacy in reducing lipid peroxidation, rebalancing apoptotic proteins, suppressing pro-inflammatory cytokines, and preserving renal histological structure. The concurrent use of lithium and astaxanthin showed a considerable amelioration of lithium-induced damage, suggesting astaxanthin's role in attenuating the nephrotoxic effects of lithium, both at a molecular and structural level. CONCLUSION: Astaxanthin demonstrates significant renoprotective effects against lithium-induced nephrotoxicity, suggesting its utility as an effective adjunctive therapy. Through its potent antioxidative, anti-inflammatory, and anti-apoptotic actions, astaxanthin effectively reduces renal damage associated with lithium treatment, underscoring its potential for enhancing renal health in patients receiving lithium therapy.
Subject(s)
Antioxidants , Kidney Diseases , Humans , Rats , Male , Animals , Antioxidants/pharmacology , Antioxidants/metabolism , Lithium/toxicity , Lithium/metabolism , Rats, Wistar , Kidney Diseases/chemically induced , Kidney Diseases/drug therapy , Kidney , Oxidative Stress , Apoptosis , XanthophyllsABSTRACT
The growing prevalence of lithium (Li) batteries has drawn public attention to Li as an emerging pollutant. The present study investigates the toxicity of Li+ on Chromochloris zofingiensis, examining physiological, biochemical and omics aspects. Results reveal hormesis effects of Li+ on C. zofingiensis growth. At Li+ concentrations below 5 mg L-1, Li+ can enhance chlorophyll content, mitochondrial activity, and antioxidant capacity, leading to increased dry cell weight and cell number. Conversely, when it exceeded 10 mg L-1, Li+ can reduce chlorophyll content, induce oxidative stress, and disrupt chloroplast and mitochondria structure and function, ultimately impeding cell growth. In addition, under 50 mg L-1 Li+ stress, microalgae optimize absorbed light energy use (increasing Fv/Fm and E TR ) and respond to stress by up-regulating genes in starch and lipid biosynthesis pathways, promoting the accumulation of storage components. Weighted gene co-expression network analysis indicates that peptidylprolyl cis/trans isomerase, GTPase and L-ascorbate oxidase might be the key regulators in response to Li+ stress. This research marks the toxic effects and molecular mechanisms of Li+ on freshwater microalga, which would improve our understanding of Li's toxicology and contributing to the establishment of Li pollution standards.
Subject(s)
Chlorophyceae , Microalgae , Antioxidants/metabolism , Microalgae/metabolism , Lithium/toxicity , Photosynthesis , Chlorophyll/metabolism , Chlorophyceae/metabolismABSTRACT
INTRODUCTION: In bipolar women who took lithium during pregnancy, several epidemiology studies have reported small increases in a rare fetal cardiac defect termed Ebstein's anomaly. METHODS: Behavioral, environmental, and lifestyle-associated risk factors associated with bipolar disorder and health insurance status were determined from an Internet search. The search was conducted from October 1, 2023, through October 14, 2023. The search terms employed included the following: bipolar, bipolar disorder, mood disorders, pregnancy, congenital heart defects, Ebstein's anomaly, diabetes, hypertension, Medicaid, Medicaid patients, alcohol use, cigarette smoking, marijuana, cocaine, methamphetamine, narcotics, nutrition, diet, obesity, body mass index, environment, environmental exposures, poverty, socioeconomic status, divorce, unemployment, and income. No quotes, special fields, truncations, etc., were used in the searches. No filters of any kind were used in the searches. RESULTS: Women who remain on lithium in the United States throughout their pregnancy are likely to be experiencing mania symptoms and/or suicidal ideation refractory to other drugs. Pregnant women administered the highest doses of lithium salts would be expected to have been insufficiently responsive to lower doses. Any small increases in the retrospectively determined risk of fetal cardiac anomalies in bipolar women taking lithium salts cannot be disentangled from potential developmental effects resulting from very high rates of cigarette smoking, poor diet, alcohol abuse, ingestion of illegal drugs like cocaine or opioids, marijuana smoking, obesity, and poverty. CONCLUSIONS: The small risks in fetal cardiac abnormalities reported in the epidemiology literature do not establish a causal association for lithium salts and Ebstein's anomaly.
Subject(s)
Cocaine , Ebstein Anomaly , Teratogenesis , Humans , Pregnancy , Female , Lithium/toxicity , Ebstein Anomaly/chemically induced , Ebstein Anomaly/epidemiology , Teratogens , Salts , Retrospective Studies , Antimanic Agents , Obesity/epidemiology , Obesity/chemically inducedABSTRACT
The growing use of lithium (Li) in industrial and energy applications and increasing demand worldwide has inevitably resulted in its wide dispersal, representing a significant threat to aquatic systems. Unfortunately, as a ubiquitous emerging contaminant, the comprehensive toxicological information regarding Li at multifarious levels is limited. To diminish this gap, this work was focused to explore Li-induced cascading effects on Daphnia magna as a key species in freshwater ecosystems. Specifically, the organisms were chronically exposed to gradient Li concentrations with emphasis on characterizing life-history traits from individual to population scale, primarily as observed by a markedly concentration-dependent decrease along exposure gradients. In parallel, a robust set of biomarkers relating to energy reserves, antioxidant and biotransformation enzymes, cellular damage, ionoregulation and neurotoxicity were assayed for further understanding potential underlying mechanisms. As a result, biomarker alterations were characterized by significant decreases in energy storage and enzymatic profiles of antioxidant and biotransformation systems, not only triggering an imbalance between reactive oxygen species (ROS) generation and elimination under Li exposure, but compromising the fecundity fitness of phenotypical costs. In contrast, malondialdehyde (MDA) levels were remarkably enhanced as a consequence of inefficient antioxidant and biotransformation capacity leading to lipid peroxidation (LPO). Additionally, Li exerted a dose-dependent biphasic effect on the activities of superoxide dismutase (SOD), Na+,K+-ATPase and acetylcholinesterase (AChE) by interfering with inherent balance. In terms of responsive patterns and dose-effect trends, the integrated biomarker response indices (IBRv2) and star plots were consistent with the differences in biomarker profiles, not only presenting comprehensively biological effects in a visualized form, but signaling the importance of progressive induced changes in an integrative way. Overall, these findings highlighted the need for elucidating Li-produced impacts from a comprehensive perspective, providing valuable insights into better understanding the toxicity of Li in relation to aquatic ecosystem functioning and ecological relevance.
Subject(s)
Antioxidants , Water Pollutants, Chemical , Animals , Antioxidants/metabolism , Lithium/toxicity , Daphnia magna , Oxidative Stress , Ecosystem , Acetylcholinesterase/metabolism , Daphnia , Biomarkers/metabolism , Water Pollutants, Chemical/metabolismABSTRACT
Boron neutron capture therapy is a perspective selective technology for the destruction of cancer cells, while the use of lithium instead of boron may represent a new and promising vector for the development of neutron capture therapy (NCT). The aim of the study was a comparative assessment of the cytotoxicity of various lithium salts, as well as an analysis of the accumulation of lithium in tumor cells in vitro to determine the possibility of using lithium in NCT. The cytotoxicity of lithium salts was determined using MTT-test and colony forming assay on human fibroblasts BJ-5ta, human skin melanoma SK-Mel-28, and mouse skin melanoma B16 cell lines. An assessment of lithium concentration in cells was performed using inductively coupled plasma atomic emission spectrometry. Our results showed that three different lithium salts at a concentration of 40 µg/ml are not toxic for both tumor and normal cells. The highest uptake values were obtained on murine melanoma B16 cells when exposed to lithium carbonate (0.8 µg/106 cells); however, human melanoma SK-Mel-28 cells effectively accumulated both lithium carbonate and lithium citrate (about 0.46 µg/106 cells for two salts). Thus, our results demonstrate a range of non-toxic doses of lithium salts and a high uptake of lithium by tumor cells, which indicates the possibility to use the lithium in NCT.
Subject(s)
Boron Neutron Capture Therapy , Melanoma , Mice , Humans , Animals , Melanoma/drug therapy , Melanoma/metabolism , Melanoma/pathology , Lithium/toxicity , Salts , Lithium Carbonate/toxicity , Boron Neutron Capture Therapy/methodsABSTRACT
Epilepsy is a chronic neurological complication characterized by unprovoked seizure episodes due to the imbalance between excitatory and inhibitory neurons. The epileptogenesis process has been reported to be involved in chronic epilepsy however, the mechanism underlying epileptogenesis remains unclear. Recent studies have shown the possible involvement of Wnt/ß-catenin signaling in the neurogenesis and neuronal reorganization in epileptogenesis. In this study, we used repeated low dose lithium-pilocarpine model of status epilepsy (SE) to study the involvement of Wnt/ß-catenin signaling at acute and chronic stages post SE induction. The acute study ranged from day 0 to day 28 post SE induction and the chronic study ranged from day 0 to day 56 post SE induction. Several neurobehavioral parameters and seizure score and seizure frequency was analysed until the end of the study. The proteins involved in the regulation of Wnt/ß-catenin signaling and downstream cascading were analysed using western blot and quantitative real-time PCR analysis. The Wnt/ß-catenin pathway was found inactive in acute SE, while the same was found activated at the chronic stage. Our findings suggest that the activated Wnt/ß-catenin signaling in chronic epilepsy might be the possible mechanism underlying epileptogenesis as indicated by increased neuronal count, increased synaptic density, astrogliosis and apoptosis in chronic epilepsy. These findings can help target the Wnt/ß-catenin pathway differentially depending upon the type of epilepsy. The acute stage characterized by SE can be improved by targeting GSK-3ß levels and the chronic stage characterized by temporal lobe epilepsy can be improved by targeting ß-catenin and disheveled proteins.
Subject(s)
Epilepsy , Status Epilepticus , Rats , Animals , Pilocarpine/toxicity , Lithium/toxicity , beta Catenin/metabolism , Glycogen Synthase Kinase 3 beta/metabolism , Epilepsy/chemically induced , Epilepsy/metabolism , Status Epilepticus/chemically induced , Status Epilepticus/metabolism , Seizures/metabolism , Hippocampus/metabolism , Disease Models, AnimalABSTRACT
Lithium (Li) salts are commonly used as medications for bipolar disorders. In addition to its therapeutic value, Li is also being increasingly used as a battery component in modern electronic devices. Concerns about its toxicity and negative impact on the heart have recently been raised. We investigated the effects of long-term Li treatment on the heart, liver, and kidney in mice. Sixteen C57BL/6J mice were randomly assigned to receive oral administration of Li carbonate (n = 8) or act as a control group (n = 8) for 12 weeks. We evaluated the cardiac electrical activity, morphology and function, and pathways contributing to remodelling. We assessed the multi-organ toxicity using histopathology techniques in the heart, liver, and kidney. Our findings suggest that mice receiving Li had impaired systolic function and ventricular repolarisation and were more susceptible to arrhythmias under adrenergic stimulation. The Li treatment caused an increase in the cardiomyocytes' size, the modulation of the extracellular signal-regulated kinase (ERK) pathway, along with some minor tissue damage. Our findings revealed a cardiotoxic effect of Li at therapeutic dosage, along with some histopathological alterations in the liver and kidney. In addition, our study suggests that our model could be used to test potential treatments for Li-induced cardiotoxicity.
Subject(s)
Antimanic Agents , Lithium , Mice , Animals , Lithium/toxicity , Mice, Inbred C57BL , Antimanic Agents/therapeutic use , Lithium Compounds , Cardiotoxicity/drug therapyABSTRACT
Lithium (Li) has been widely used in clinical therapy and new Li-ion battery industry. To date, the impact of Li on the development of immune cells is largely unknown. The aim of this study was to investigate the impact of Li on hematopoiesis. C57BL/6 (B6) mice were treated with 50 ppm LiCl, 200 ppm LiCl, or the control via drinking water for 3 months, and thereafter the hematopoiesis was evaluated. Treatment with Li increased the number of mature lymphoid cells while suppressing the number of mature myeloid cells in mice. In addition, a direct action of Li on hematopoietic stem cells (HSC) suppressed endoplasmic reticulum (ER) stress to reduce the proliferation of HSC in the bone marrow (BM), thus leading to fewer HSC in mice. On the other hand, the suppression of ER stress by Li exposure increased the expression of Hsp90, which promoted the potential of lymphopoiesis but did not impact that for myelopoiesis in HSC in the BM of mice. Moreover, in vitro treatment with Li also likely disturbed the ER stress-Hsp90 signaling, suppressed the proliferation, and increased the potential for lymphopoiesis in human HSC. Our study reveals a previously unrecognized toxicity of Li on HSC and may advance our understanding for the immunotoxicology of Li.
Subject(s)
Hematopoietic Stem Cells , Lithium , Animals , Humans , Mice , Bone Marrow , Hematopoiesis , Hematopoietic Stem Cells/metabolism , Lithium/toxicity , Mice, Inbred C57BLSubject(s)
Globus Pallidus , Lithium , Humans , Globus Pallidus/diagnostic imaging , Globus Pallidus/injuries , Lithium/toxicityABSTRACT
Status Epilepticus (SE) is a distributed network disorder, which involves the hippocampus and extra-hippocampal structures. Epileptogenesis in SE is tightly associated with neurogenesis, plastic changes and neural network reorganization facilitating hyper-excitability. On the other hand, dendritic spines are known to be the excitatory synapse in the brain. Therefore, dendritic spine dynamics could play an intricate role in these network alterations. However, the exact reason behind these structural changes in SE are elusive. In the present study, we have investigated the aforementioned hypothesis in the lithium-pilocarpine treated rat model of SE. We have examined cytoarchitectural and morphological changes using hematoxylin-eosin and Golgi-Cox staining in three different brain regions viz. CA1 pyramidal layer of the dorsal hippocampus, layer V pyramidal neurons of anterior temporal lobe (ATL), and frontal neocortex of the same animals. We observed macrostructural and layer-wise alteration of the pyramidal layer mainly in the hippocampus and ATL of SE rats, which is associated with sclerosis in the hippocampus. Sholl analysis exhibited partial dendritic plasticity in apical and basal dendrites of pyramidal cells as compared to the saline-treated weight-/age-matched control group. These findings indicate that region-specific alterations in dendritogenesis may contribute to the development of independent epileptogenic networks in the hippocampus, ATL, and frontal neocortex of SE rats.
Subject(s)
Neocortex , Status Epilepticus , Rats , Animals , Pilocarpine/toxicity , Lithium/toxicity , Disease Models, Animal , Hippocampus , Status Epilepticus/chemically induced , Temporal LobeABSTRACT
Lead (Pb) and lithium (Li) are metals which have been detected in the environment and, at high concentrations, can induce toxic effects that disturb the growth, metabolism or reproduction of organisms along the entire trophic chain. The impacts of these metals have scarcely been investigated using marine bivalves, especially when acting as a mixture. The present study aimed to investigate the influence of temperature on the ecotoxicological effects caused by Pb and Li, acting alone and as a mixture, on the mussel species Mytilus galloprovincialis after 28 days of exposure. The impacts were evaluated under actual (17 °C) and projected (+4 °C) warming conditions, to understand the influence of temperature rise on the effects of the metals (both acting alone or as a mixture). The results obtained showed that the increased temperature did not influence the accumulation of metals. However, the biomarkers evaluated showed greater responses in mussels that are exposed to metals under increased temperature (21 °C). The IBR index showed that there is a comparable toxic effect of Li and Pb separately, while exposure to a mixture of both pollutants causes a significantly higher stress response. Overall, the results obtained revealed that temperature may cause extra stress on the mussels and exposure to the metal mixture caused the greatest impacts compared to each metal acting alone.
Subject(s)
Mytilus , Water Pollutants, Chemical , Animals , Temperature , Lithium/toxicity , Lead/toxicity , Lead/metabolism , Mytilus/physiology , Water Pollutants, Chemical/analysis , Oxidative Stress , Biomarkers/metabolismABSTRACT
Lithium (Li) is present in many modern technologies, most notably in rechargeable batteries. Inefficient recycling strategies for electronic waste containing this element may result in its release into aquatic systems, which may induce harmful effects on wildlife. The present study evaluated the effect of Li contamination on the gastropod Tritia reticulata exposed to different concentrations of Li (100, 200, 500 and 1000 µg L-1) for 21 days. Biochemical analyses showed that this species was not significantly affected by this contaminant at the cellular level, as no significant differences were observed in terms of metabolism, oxidative stress, and neurotoxicity. Results further revealed that snails attempted to avoid Li accumulation by burying in the sediment at a faster rate when exposed to the highest concentrations (500 and 1000 µg L-1). More research is needed to fully assess the response of T. reticulata to Li contamination, such as investigating longer exposure periods or other endpoints.
Subject(s)
Lithium , Snails , Water Pollutants, Chemical , Animals , Lithium/toxicity , Lithium/metabolism , Oxidative Stress , Snails/physiology , Water Pollutants, Chemical/toxicity , Electronic WasteABSTRACT
Lithium (Li) is now widely used in green energies/clean technologies; however, due to its inefficient recycling and treatment, it is an emerging contaminant in aquatic systems. Bivalves, such as clams, are considered good bioindicators of pollution, hence we evaluated the biochemical effects of Li in the clam Venerupis corrugata. Clams were exposed (14 days) to an increasing Li gradient (0, 200, 400, 800 µg/L). Bioconcentration capacity tended to decrease with increasing Li exposure possibly due to efforts to eliminate Li from the cells, to avert damage. No influences on the clams' metabolic capacity and protein content were observed. Antioxidant and detoxification defences were activated, especially at 400 and 800 µg/L of Li, avoiding lipid damage, while protein injuries were observed at higher concentrations. Furthermore, a loss of redox balance was observed. This study highlights the importance of preventing and regulating Li discharges into the environment, avoiding adverse consequences to aquatic ecosystems.
Subject(s)
Bivalvia , Water Pollutants, Chemical , Animals , Lithium/toxicity , Lithium/metabolism , Oxidative Stress , Ecosystem , Biomarkers/metabolism , Bivalvia/metabolism , Water Pollutants, Chemical/analysisABSTRACT
Las intoxicaciones en nuestro medio se presenta con una incidencia de 45.1 por cada 100,000 habitantes. Una de las principales causas son las intoxicaciones por psicofármacos dentro de las cuales esta el litio. Este medicamento es utilizado para el manejo del trastorno afectivo bipolar. En la literatura existen diferentes factores de riesgo para la intoxicación por litio como: condiciones que favorezcan la hipovolemia, uso de diuréticos, antihipertensivos, hiponatremia , interacciones medicamentosas y ajuste de dosis. Alrededor del 75 a 90% de los pacientes tratados crónicamente con litio pueden tener niveles tóxicos durante su tratamiento. Como tal la intoxicación puede cursar con diferentes complicaciones renales, cardiovasculares y neurológicas, dentro de estas últimas ésta la encefalopatía. Presentamos el caso de una paciente que ingresa con toxicidad crónica y presenta como complicación neurológica una encefalopatía posterior reversible. El objetivo de este reporte es sensibilizar al personal medico sobre esta complicación poco frecuente pero asociada a gran morbimortalidad. (AU)
Intoxications in our enviroment has an incidence of 45.1 for each 100.000 habitants. One of the main causes are psychopharmaceuticals, one of which is lithium. This drug is used in the management of bipolar disorder. There are several risk factors depicted on literature for this intoxication, such as: conditions that favor hipovolemia, diurethic and antihypertensive use, hiponatremia, drug interactions and lithium dose adjustment. About 75 to 90% of patients chronically treated with lithium can reach toxic levels during their treatment. Lithium intoxication can present with complications affecting different systems such as renal, cardiovascular and nervious, last one includying encephalopathy. We will discuss the case of a patient that presents with chronic lithuim toxicity and develops posterior reversible encephalopathy as a neurologic complication. The goal of this case report is to sensitize medical staff with this unfrequent but dangerous complication. (AU)
Subject(s)
Humans , Female , Middle Aged , Lithium/toxicity , Poisoning/complications , Brain Diseases , Bipolar Disorder/drug therapyABSTRACT
Lithium (Li) is a toxic monovalent alkaline metal used in household items common to industrial applications. The present work was aimed at investigating the potential toxic effects of LiCl on the redox status, fatty acid composition, and histological aspects of the marine ragworm Perinereis cultrifera. Sea worms were exposed to LiCl graded doses (20, 40, and 80 mg/L) for 48 h. Compared with the control group, the saturated fatty acids (SFA) decreased while monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA) increased upon exposure to LiCl. The increase in PUFA n-3 and PUFA n-6 was concomitant to an increase in docosahexaenoic (DHA: C22:6n-3), eicosapentaenoic (EPA: C20:5n-3), and docosapentaenoic acid (C22:5n-6) fatty acids. Results showed that LiCl-treated specimens accumulate lithium with increasing exposure gradient. Indeed, the exposure to LiCl doses promoted oxidative stress with an increase of the ferric reducing antioxidant power (FRAP), malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein product (AOPP), and protein carbonyl (PCO) as well as the enzymatic and non-enzymatic antioxidants (non-protein thiols (NPSH), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST), and metallothionein (MT)) levels in all treated groups. Our biochemical findings have been affirmed by the histopathological observations showing hyperplasia and loss of the intestine structure in treated specimens. Overall, our findings give new insights on the toxic effect of LiCl on the redox status of P. cultrifera body tissue and highlighted the usefulness of the FA composition as an early sensitive bioindicators to better understand LiCl mechanism of toxicity in marine polychaetes.