Fluoride-induced Toxicity Research Articles

Hematological Response of Clarias batrachus to Sodium Fluoride-Induced Toxicity

Hematological Response of Clarias batrachus to Sodium Fluoride-Induced Toxicity

Hepatotoxic alterations due to sodium fluoride-induced toxicity in Clarius batrachus

Although fluoride can be found in nature in a variety of forms and has been widely used in different products. The amount of fluoride higher than the permissible limit is toxic to liver. Fluoride in drinking water in excess (>1.5 mg/l) is unhealthy. Given that fluoride toxicity has been classified as an endemic factor for liver diseases in several nations. It is crucial to pay close attention to the precise toxic effects of fluoride on different aquatic animals. Fluoride is toxic to all the system and causes oxidative stress in various tissues and has been demonstrated to have a number of negative consequences on human and aquatic health. The study was conducted to observe the hepatotoxicity in C. batrachus due to fluoride exposure. Changes in behavior could be read as exact indicators of a stressful environment. Fish are an efficient bioindicator of a hazardous environment because they can absorb fluoride from food and water. The toxicity of sodium fluoride (NaF) in fish was evaluated after acute exposure for 10 days. To evaluate the hepatotoxicity caused due to fluoride exposure three groups were set up, control, high dose (87.48 mg/l), and low dose (34.975 mg/l). The behavioral and biochemical parameters in the liver were evaluated. Results show that a high dose of fluoride is more toxic to the liver in contrast to the control group. Characteristic behavioral changes such as hyperactivity, frequent surfacing activity, a vertical swimming pattern, a high heart rate, and low oxygen saturation were observed in C. batrachus.

Effects of Fluoride Exposure on Thiol/ Disulphide Homeostasis, Testicular Oxidative Stress and Histopathological Changes in Rats

Objective: This study investigated the effects of fluoride-induced toxicity on the reproductive system. For this purpose, testicular oxidative stress, thiol/disulpide homeostasis, sperm motility, density, and histopathology of testicular tissue were evaluated. Material and Methods: In the experiment, 4 groups were formed, with eight animals (n=8) in each group. Group 1, control/saline, groups 2, 3, and 4 were administered orally sodium fluoride (NaF) at doses of 25, 50, and 100 ppm, respectively, for 30 days. Then the rats were sacrificed and testicular tissue samples were evaluated by sperm examination and histopathologically. Biochemical parameters malondialdehyde (MDA), catalase (CAT), advanced oxidation, and protein products (AOPP) were measured spectrometrically. Thiol/disulphide homeostasis was studied with a fully automated analysis method. Results: NaF exposure increased MDA and AOPP levels and decreased CAT levels. Disrupted thiol/disulphide homeostasis. Histopathological examination revealed integrity between germinal cells and tubular atrophy. NaF showed reduced sperm motility and density and increased abnormal sperm count. The findings of the NaF 100 ppm group were statistically significant when compared with the Control and other NaF groups (p˂0.05). Conclusion: The findings concluded that fluoride might cause pathological conditions and infertility in testicular tissue.

Phytol as a hepatoprotective compound in the leaves of Eichhornia crassipes

Water hyacinth is undoubtedly an environmental problem due to its invasiveness, but it also has some promising futures. It might be preferable to consider the specific attributes of each environment where the plant grows. When there are facilities available to fully utilize this plant's potential, efforts should be focused on maximizing its growth. It has been shown that secondary metabolites, such as phenolic and anti-oxidant components, play a crucial role in the chemical defenses of plants against invaded microscopic organisms. This test was conducted to analyze whether Eichhornia crassipes leaves contained antioxidants or the hepatoprotectant. The ethyl acetate-fractionated hydroethanolic extract was used for the analysis. Using Gas Chromatography-Mass Spectrometer (GC-MS), and High-Pressure Liquid Chromatography, the bioactive components of the ethyl acetate fraction of the hydroethanolic extract of the leaves of E. crassipes (Mart.) Solms were analyzed. The GC-MS analysis of the extract revealed the presence of phytol, a constituent that is essential for hepatoprotection. The human body needs phytol for its benefits. Phytol may also be considered a potential new drug and treatment for hepatic dysfunction. The numerous substances found in plants used in traditional medicine can be used to treat several ailments. The majority of people follow traditional medicine, which contains substances derived from medicinal plants, is practiced. Therefore, research into these plants is necessary to better understand their characteristics, safety, and effectiveness. Hence, the present work aimed to evaluate the protective efficacy of the leaf extract of E. crassipes against fluoride-induced toxicity.

Glutathione S-transferase genetic polymorphisms and fluoride-induced reproductive toxicity in men with idiopathic infertility.

Male infertility caused by idiopathic oligoasthenospermia (OAT) is known as idiopathic male infertility. Glutathione S-transferase (GST) and fluoride may play important roles in idiopathic male infertility, but their effects are still unknown. Our study examined the relationship between GST polymorphisms and fluoride-induced toxicity in idiopathic male infertility and determined the underlying mechanism. Sperm, blood, and urine samples were collected from 560 males. Fluoride levels were measured by a highly selective electrode method, and GST genotypes were identified using polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP). Semen parameters, DNA fragmentation index (DFI), mitochondrial membrane potential (MMP), and oxidative stress (OS) biomarkers were statistically assessed at the P < 0.05 level. Compared with healthy fertile group, semen parameters, fluoride levels, OS biomarkers, sex hormone levels, and MMP and DFI levels were lower in the idiopathic male infertility group. For glutathione S-transferase M1 (GSTM1[-]) and glutathione S-transferase T1 (GSTT1[-]) or glutathione S-transferase P1 (GSTP1) mutant genotypes, levels of semen fluoride, OS, MMP, and DFI were considerably higher, and the mean levels of sperm parameters and testosterone were statistically significant in GSTM1(+), GSTT1(+), and GSTP1 wild-type genotypes. Both semen and blood fluoride levels were associated with oxidative stress in idiopathic male infertility patients. Elevated fluoride in semen with the genotypes listed above was linked to reproductive quality in idiopathic male infertility patients. In conclusion, GST polymorphisms and fluorine may have an indicative relationship between reproductive quality and sex hormone levels, and OS participates in the development of idiopathic male infertility.

Effects of Fluoride on Metabolic enzymes of brain and Gastrocnemius muscle of mice: protective role of selenium and alpha-tocopherol

The present study aimed to investigate the ameliorative effects of Selenium and Alpha-tocopherol on activities of enzymes involved in metabolic functions, energy production and transfer in the brain and gastrocnemius muscle of mice treated with sodium fluoride. Animals were separated into five groups and treated with Selenium (05 µg/kg BW), Alpha-tocopherol (2mg/kg BW) alone, and in combination for 15 days to evaluate their ameliorative effects against fluoride (20mg/kg BW) toxicity. The obtained results showed a statistically significant (p&lt;0.05) decrease in the body weight, organo-somatic index, protein content, ALAT, AAT, CPK, acid phosphatase and alkaline phosphatase enzymes activities in the fluoride-treated group in comparison with control group indicates oxidative stress induced by fluoride. The effect of fluoride on enzymes of muscle was comparatively higher, which suggests the greater accumulation of fluoride in muscle than brain. These changes were reverted moderately in Selenium and alpha-tocopherol alone treated groups, and significantly (p&lt;0.05) in Selenium + alpha-tocopherol treated group suggests the combinatorial effect of Selenium and alpha-tocopherol in the amelioration of fluoride-induced toxicity. In conclusion, the findings all pointed to the fact that Selenium and alpha-tocopherol showed combinatorial effects in the amelioration of oxidative stress induced by fluoride.

Gene expression and alterations of antioxidant enzymes in spleen of rats exposed to fluoride

BackgroundFluorosis is a slow and progressive process causing metabolic, functional and structural damages affecting many tissues particularly musculoskeletal, dental systems, kidney, liver and brain. It can be rapidly absorbed by passive diffusion through the stomach, small intestine, mouth and skin. Endemic fluorosis is connected to the high concentration of fluoride in drinking water. The present study aimed to evaluate the toxic effects of sodium fluoride (NaF) on splenic activity at the biochemical and molecular level. Materials and methodsWistar albino rats were randomly assigned to three groups. The control rats were given 1 ml deionized water orally for 40 days. Groups II and III were administered 300 and 600 mg NaF/kg b.w. /day for the same period. Animals were sacrificed under ether anaesthesia. The spleen tissue was excised and used for biochemical and real-time PCR analysis. The level of fluoride, malondialdehyde (MDA), reduced glutathione (GSH) and activities of different antioxidant enzymes such as cytosolic copper/zinc superoxide dismutase (Cu/Zn SOD), glutathione peroxidase (GPx) and catalase (CAT) were determined. The analysis of gene expression of Cu/Zn SOD, GPx and CAT in spleen was done using Real-time PCR. ResultsThe levels of fluoride and MDA were significantly (P < 0.0001) increased where as GSH content decreased significantly (P < 0.0001) in the spleen of fluoridated rats. The activities of antioxidant enzymes viz; Cu/Zn SOD, GPx and CAT declined significantly (P < 0.0001) compared to the control. Pearson’s bivariate correlation and simple linear regression analysis exhibited strong positive correlation between levels of splenic tissue fluoride and MDA(r = 0.985) while negative correlations existed in GSH (r = −0.907) as well as activities of Cu/Zn SOD (r = −0.982), GPx (r = −0.966), and CAT (r = −0.935). The gene expression of Cu/Zn SOD, GPx and CAT were significantly (P < 0.0001) reduced in fluorotic rats. ConclusionIt is concluded that fluoride intoxication leads to the development of oxidative stress and damaging the cellular metabolism resulting in the declined ability of free radical scavengers along with increased level of MDA and decreased expression level of antioxidant genes which helps to understand the possible mechanism of fluoride-induced toxicity at the molecular level.

Selenomethionine alleviated fluoride-induced toxicity in zebrafish (Danio rerio) embryos by restoring oxidative balance and rebuilding inflammation homeostasis.

Fish are target organisms that are extremely susceptible to fluoride pollution, and an increase in fluoride load will damage multiple systems of fish. Selenomethionine (Se-Met) at low levels has been reported to alleviate oxidative damage and inflammation caused by toxic substances, but whether it can alleviate fluoride-induced toxicity in zebrafish embryos has not been elucidated. In this study, the intervention effects of Se-Met on developmental toxicity, oxidative stress and inflammation in zebrafish embryos exposed to fluoride were determined. Our results showed that fluoride accumulated in larvae and induced developmental toxicity in zebrafish embryos, caused oxidative damage and apoptosis, increased significantly the MPO and LZM activities and the levels of the inflammation-related genes IL-1β, IL-6, TNF-α, IL-10 and TGF-β. Moreover, fluoride significantly increased the levels of ERK2, JNK, p38 and p65 in MAPKs and NF-κB pathways. Se-Met-treatment alleviated the adverse effects induced by fluoride, and all of the above indicators induced by fluoride returned to near control levels with increasing concentrations and time. However, treatment with Se-Met-alone also markedly increased the levels of IL-6, TNF-α, IL-10, TGF-β, ERK2 and JNK. In short, these data demonstrated that Se-Met-could alleviate fluoride-induced toxicity in zebrafish embryos by restoring oxidative balance and rebuilding inflammation homeostasis, although low levels of Se-Met-alone had certain toxic effects on zebrafish embryos. Taken together, Se-Met-plays an important role in preventing toxic damage induced by fluoride in zebrafish embryos, although it has certain toxic effects.

Alleviate Effect of Pomegranate Peel Extract in Ameliorating Fluoride-Induced Cytotoxicity, Oxidative Stress in Tetrahymena pyriformis Model

Fluoride is a major oligo element found in nature, at excessive amounts can cause enormous harm in mammalian cells. Fruits peel, considered most often as a waste of juice processing, could play an important role in attenuating metal cytotoxicity. The present study evaluated the effect of pomegranate peel (Punica granatum. L) methanolic extract (PPE) on the Fluoride-induced toxicity and redox status in the protozoa Tetrahymena pyriformis. Polyphenols of peel extract were extracted using methanol and characterized by spectrophotometric methods, total phenolic content (TPC), total flavonoids content (TFC), and in vitro, antioxidant properties were assessed using the Folin-Ciocalteu method and DPPH, ABTS, and FRAP. Pomegranate peel is a rich source of phenolic compounds TP (223.21 ± 15 mg GAE/g dw), TF (52.12 ± 1.36 mg Qu/g dw) and showed high antioxidant properties DPPH (EC50 0.043 ± 0.06 mg/ml), ABTS (EC50 0.06 ± 0.01 mg/ml) and FRAP (1.47 ± 0.01 mg AA equivalents/g dw). Cells were incubated with fluoride alone and in combination with PPE. NaF (0.8 mM) significantly decreased the cell viability, induced oxidative stress by decreasing antioxidants enzyme activities, and increased intracellular fluoride content. Treatment with NaF in combination with PPE decreases CAT, SOD, and GPx activities and alleviates GSH content. These findings suggest that pomegranate peel biomolecules may have a protective effect against fluoride induced-toxicity.

Toxic effects of fluoride in intestinal epithelial cells and the mitigating effect of methanol extract of coconut haustorium by enhancing de novo glutathione biosynthesis

Fluoride ions are an important environmental contaminant and pollutant found in a wide variety of environmental conditions. The fluoride in drinking water is evident to induce toxic effects including neurodegeneration, skeletal and dental fluorosis as well as organ damage. Nutraceuticals and functional foods are emerging as possible preventive agents against fluoride toxicity. Hence, the possible use of an emerging functional food-the coconut haustorium is being evaluated against sodium fluoride-induced toxicity in intestinal cells (IEC-6). The cells exposed to fluoride showed significant cell death mediated through the increased lipid peroxidation and glutathione depletion. The glutathione biosynthetic enzymes were inhibited by the exposure to fluoride and the apoptotic genes (caspases 3/7 and apaf-1) were upregulated. The CHE pre-treatment improved the activity of enzymes involved in the de novo biosynthesis of glutathione and subsequently improved the intracellular GSH pool. The improved antioxidant defense was also evident from the reduced expression of apoptotic genes (p < 0.05). Overall, the study concludes that fluoride ions induce oxidative stress-mediated apoptosis in intestinal epithelial cells, via inhibiting glutathione biosynthesis. Methanol extract of coconut haustorium increased glutathione biosynthesis and subsequently prevented fluoride toxicity in IEC-6 cells by virtue of its antioxidant potentials.

Fluoride-induced toxicity is ameliorated in a susceptible indica rice cultivar by exogenous application of the nitric oxide donor, sodium nitroprusside

Fluoride-induced toxicity is ameliorated in a susceptible indica rice cultivar by exogenous application of the nitric oxide donor, sodium nitroprusside

Hesperidin protects liver and kidney against sodium fluoride-induced toxicity through anti-apoptotic and anti-autophagic mechanisms

AimHigh dose of fluoride intake is associated with toxic effects on liver and kidney tissues. One approach to tackle these toxicities is using natural antioxidants as supplements. This study evaluated the ameliorative effects of hesperidin (HSP) against sodium fluoride (NaF)-induced hepatotoxicity and nephrotoxicity in wistar albino rats. Materials and methodsIn the present study, the rats were randomly allocated into five groups of seven male rats each group: control, NaF (600 ppm), HSP-200, NaF + HSP-100 and NaF + HSP 200. Key findingsHepatic and renal injuries induced by NaF were confirmed by the alteration in kidney function parameters in the serum (urea and creatinine), levels of liver enzymes (ALT, ALP and AST), activities of the antioxidant enzymes (SOD, CAT and GPx) and levels of inflammatory markers (NF-κB, IL-1β and TNF-α). NaF also inhibited PI3K/Akt/mTOR pathway, increased levels of autophagic markers (Beclin-1, LC3A and LC3B) and expression levels of apoptotic and anti-apoptotic proteins (Bax, Bcl-2, cytochrome c, p53 and procaspase-3) in the liver and kidney tissues. Administration of HSP concurrently with NaF significantly ameliorated the deviation in the above-studied parameters. SignificanceThe results of the current study revealed that HSP could be used as a beneficial adjuvant that confers protection against NaF-induced liver and kidney damage through antioxidant, anti-inflammatory, anti-apoptotic and anti-autophagic mechanisms.

Curcumin suppresses cell growth and attenuates fluoride-mediated Caspase-3 activation in ameloblast-like LS8 cells.

The trace element fluoride can be beneficial for oral health by preventing dental caries. However, fluoride is also known as an environmental pollutant. Fluoride pollution can lead to fluoride over-ingestion and can cause health issues, including dental fluorosis. Curcumin attenuated fluoride-induced toxicity in animal models, however the molecular mechanisms of how curcumin affects fluoride toxicity remain to be elucidated. We hypothesized that curcumin attenuates fluoride toxicity through modulation of Ac-p53. Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity. LS8 cells were treated with NaF with/without curcumin. Curcumin significantly increased phosphorylation of Akt [Thr308] and attenuated fluoride-mediated caspase-3 cleavage and DNA damage marker γH2AX expression. Curcumin-mediated attenuation of caspase-3 activation was reversed by Akt inhibitor LY294002 (LY). However, LY did not alter curcumin-mediated γH2AX suppression. These results suggest that curcumin inhibited fluoride-mediated apoptosis via Akt activation, but DNA damage was suppressed by other pathways. Curcumin did not suppress/alter fluoride-mediated Ac-p53. However, curcumin itself significantly increased Ac-p53 and upregulated p21 protein levels to suppress cell proliferation in a dose-dependent manner. Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. However, curcumin did not reverse fluoride-mediated cell growth inhibition. These results suggest that curcumin-induced Ac-p53 and p21 led to cell cycle arrest, while curcumin attenuated fluoride-mediated apoptosis via activation of Akt and suppressed fluoride-mediated DNA damage. By inhibiting DNA damage and apoptosis, curcumin may potentially alleviate health issues caused by fluoride pollution. Further studies are required to better understand the mechanism of curcumin-induced biological effects on fluoride toxicity.

Effect of hesperidin on fluoride-induced neurobehavioral and biochemical changes in rats.

Fluoride is the second largest contaminant of drinking water. Fluoride toxicity is a major concern in the endemic areas where a high amount of fluoride is present in ground water. Oxidative stress has been proposed to be one of the mechanisms of fluoride-induced toxicity. Antioxidant-rich food has been found to alleviate fluoride-induced toxicity. Therefore, in this study, we have examined the effect of hesperidin on fluoride-induced neurobehavioral changes in rats. In the current study, male Sprague-Dawley rats were exposed to sodium fluoride through drinking water (120 ppm). Hesperidin (200 mg kg-1 d-1 ; per os) was administered either alone or in combination with fluoride-containing drinking water. Bisphinol A diglycidyl ether (BADGE) was used as peroxisome proliferator-activated receptor-γ (PPAR-γ) antagonist and was administered (10 mg kg-1 d-1 ; intraperitoneal injection) with/without hesperidin along with fluoride-containing drinking water. The behavioral changes in the animals were assessed by analyzing rotarod test, novel object recognition test, and forced swim test (FST). After 8 weeks, animals were killed to isolate blood and brain for monitoring biochemical changes. The 8-week exposure of fluoride resulted in motor impairment as observed with reduced fall time in rotarod test, memory impairment as observed with reduced preference index in novel object recognition test, and depression-like behavior as observed with reduced mobility index in the FST. Treatment with hesperidin improved neurobehavioral impairment along with restoration in brain biochemical changes (ie, acetylcholinesterase activity and antioxidant and oxidative stress parameters). The protective effect of hesperidin was reversed by coadministration of BADGE. The neuroprotective effect of hesperidin appears to be contributed through PPAR-γ receptor.

Gibberellic Acid-Priming Promotes Fluoride Tolerance in a Susceptible Indica Rice Cultivar by Regulating the Antioxidant and Phytohormone Homeostasis

Excessive utilization of groundwater for anthropogenic purposes has led to severe depletion of the water table, resulting in contamination of fluorides from the mineral bed. Irrigation of rice seedlings with such fluoride-infested water leads to high fluoride bioaccumulation and compromised growth physiology. In the present study, we showed that the priming of seeds with gibberellic acid 3 (GA) alleviated prolonged fluoride-induced toxicity in the fluoride-susceptible indica rice cultivar, IR-64 (grown in soil) by reducing the accumulation of the xenobiotic within the seedling biomass. The primed seeds showed improved percentage of germination during fluoride stress compared to the non-primed seeds. The stressed seedlings grown from the GA-primed seeds exhibited increased endogenous accumulation of GA and the auxin, indole-3-acetic acid which stimulated shoot and root growth and relative water content, compared to the stressed seedlings germinated from the non-primed seeds. GA-priming reduced the chlorophyll degradation, affected the homeostasis of the accessory pigments and lowered the electrolyte leakage during stress. Upon GA-priming, the fluoride-induced oxidative stress was ameliorated by an increase in proline, anthocyanin, flavonoid and total phenolic contents, reducing power, total antioxidant capacity and DPPH-radical scavenging activity. The altered activity of the antioxidative enzymes like catalase, ascorbate peroxidase and guaiacol peroxidase also enabled efficient H2O2 scavenging in the stressed plants germinated from the primed seeds. Thus, seed pre-treatment with GA promoted fluoride tolerance by activating the antioxidant machinery and elevating the endogenous level of the two most important classes of plant growth regulators, gibberellic acid and auxin.

Histone acetyltransferase promotes fluoride toxicity in LS8 cells

Previously we demonstrated that fluoride increased acetylated-p53 (Ac-p53) in LS8 cells that are derived from mouse enamel organ epithelia and in rodent ameloblasts. However, how p53 is acetylated by fluoride and how the p53 upstream molecular pathway responds to fluoride is not well characterized. Here we demonstrate that fluoride activates histone acetyltransferases (HATs) including CBP, p300, PCAF and Tip60 to acetylate p53. HAT activity is regulated by post-translational modifications such as acetylation and phosphorylation. HAT proteins and their post-translational modifications (p300, Acetyl-p300, CBP, Acetyl-CBP, Tip60 and phospho-Tip60) were analyzed by Western blots. p53-HAT binding was detected by co-immunoprecipitation (co-IP). Cell growth inhibition was analyzed by MTT assays. LS8 cells were treated with NaF with/without HAT inhibitors MG149 (Tip60 inhibitor) and Anacardic Acid (AA; inhibits p300/CBP and PCAF). MG149 or AA was added 1 h prior to NaF treatment. Co-IP results showed that NaF increased p53-CBP binding and p53-PCAF binding. NaF increased active Acetyl-p300, Acetyl-CBP and phospho-Tip60 levels, suggesting that fluoride activates these HATs. Fluoride-induced phospho-Tip60 was decreased by MG149. MG149 or AA treatment reversed fluoride-induced cell growth inhibition at 24 h. MG149 or AA treatment decreased fluoride-induced p53 acetylation to inhibit caspase-3 cleavage, DNA damage marker γH2AX expression and cytochrome-c release into the cytosol. These results suggest that acetylation of p53 by HATs contributes, at least in part, to fluoride-induced toxicity in LS8 cells via cell growth inhibition, apoptosis, DNA damage and mitochondrial damage. Modulation of HAT activity may, therefore, be a potential therapeutic target to mitigate fluoride toxicity in ameloblasts.

Ginkgo biloba ameliorates fluoride toxicity in rats by altering histopathology, serum enzymes of heme metabolism and oxidative stress without affecting brain mGluR5 gene

Background: To evaluate the therapeutic potential of Ginkgo biloba extract (GBE) in experimental model of fluorosis. Objectives: To study the protective effect of GBE in fluoride toxicity by assessment of oxidative stress, serum biochemical parameters, acetylcholinesterase (AChE) activity, histopathology and brain mGluR5 gene expression. Materials and Methods: Fifteen adult male Wistar rats were randomly assigned to 5 groups (n = 3 rats in each group). Group 1 (control) received water, Groups 2–5 were treated with 100 ppm of sodium fluoride for 30 days, while the Groups 3, 4 and 5 were GBE treated with 50 mg/kg, 100 mg/kg and 200 mg/kg body weight for 15 days, after sodium fluoride treatment for 30 days. Results: Elevated serum delta aminolevulinic acid dehydratase and delta aminolevulinic acid synthatase levels in fluoride intoxicated rats were ameliorated by various doses of GBE treatment. Elevated serum glutathione and decreased oxidized gluatathione levels observed in fluoride intoxicated rats were also ameliorated by GBE treatment but effectively at 100 mg/kg dose. Reduced AChE activity of hippocampus in fluoride-induced toxicity was reverted by 50 mg/kg of GBE whereas other doses (100 and 200 mg/kg) caused significant inhibition of AChE activity in comparison with fluoride group. Fluoride group rats showed significant reduction of mGluR5 gene expression levels whereas in all GBE treatment groups those changes Were not significantly reverted. GBE treatment to fluoride intoxicated rats almost reverted the degenerative changes in liver and kidney caused by fluorosis. Conclusion: The present study concluded beneficial effects of GBE in experimental model of fluorosis.

Spermine ameliorates prolonged fluoride toxicity in soil-grown rice seedlings by activating the antioxidant machinery and glyoxalase system.

The current manuscript presents the first report on the ameliorative roles of exogenous spermine (Spm) during prolonged fluoride-induced toxicity and oxidative damages in the susceptible rice cultivar, IR-64. The application of Spm increased the overall growth in the stressed seedlings by significantly restricting fluoride bioaccumulation within the shoots and roots. The Spm-treated stressed seedlings exhibited low chlorosis and induced activity of pyruvate dehydrogenase and nitrate reductase due to reduced accumulation and localization of reactive oxygen species (ROS) in the shoot and root. Spm-supplementation during stress reduced the levels of molecular damages by lowering malondialdehyde, electrolyte leakage and protein carbonylation, and lipoxygenase and protease activity due to effective detoxification of ROS by the antioxidants like proline, glycine-betaine, anthocyanin, flavonoids, phenolics and higher polyamines like Spm and spermidine. Excessive accumulation of the toxic methylglyoxal was reversed due to the activation of the glyoxalase system (comprising of glyoxalase I and II) and the ascorbate-glutathione cycle. Exogenous Spm also triggered the activity of superoxide dismutase, guaiacol peroxidase, glutathione peroxidase and phenylalanine ammonia lyase, which efficiently scavenged ROS in the stressed seedlings. Overall, Spm treatment mitigated the fluoride-induced injuries in IR-64 by reducing fluoride bioaccumulation and elaborately refining the various defence machineries.

The Potential Ameliorative Effects of Annona muricata (Linn) on Sodium Fluoride-Induced Toxicity on Haematological Indices and Fecundity of Adult Male Wistar Rats

The Potential Ameliorative Effects of Annona muricata (Linn) on Sodium Fluoride-Induced Toxicity on Haematological Indices and Fecundity of Adult Male Wistar Rats

A mini review of fluoride-induced apoptotic pathways

Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity.