Red blood cell glucose metabolism in human chronic fluoride toxicity

Desireddy, Saralakumari; Rao, P. Ramakrishna

doi:10.1007/bf01689512

Cited by 23 publications

(27 citation statements)

References 14 publications

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“…The increased oxidative stress in the animals may be the consequence of depletion of the antioxidant scavenger system (29,30). Our results are in accordance with previous studies showing close association between chronic fl uoride toxicity and increased oxidative stress (31,32).…”

Section: Il-6 = Interleukin-6; Tnf-α = Tumour Necrosis Factor-alpha; supporting

confidence: 94%

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Afolabi

Oyewo

Adekunle

et al. 2013

Archives of Industrial Hygiene and Toxicology

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The aim of this study was to establish the effects of fl uoride on lipid metabolism and attendant infl ammatory response by exposing rats to 50 mg L -1 and 100 mg L -1 of fl uoride through drinking water for seven weeks. Both concentrations led to hypercholesterolemia while the 100 mg L -1 concentration induced hypertriglyceridaemia. High density lipoprotein (HDL) cholesterol levels dropped in the exposed rats while interleukin 2 (IL-2) increased more than 1.5-fold (p<0.05) and IL-6 and plasma TNF-α more than 2.5 fold (p<0.05). Fluoride-exposed rats also had signifi cantly higher levels of liver malondialdehyde (MDA) and plasma lipid hydroperoxide (LOOH) but lower plasma paraoxonase (PON1) activity. Oxidative stress indices correlated with pro-infl ammatory cytokines and plasma cholesterol. In contrast, proinfl ammatory cytokines inversely correlated with plasma triglyceride, HDL cholesterol and PON1. Our results suggest that the association between fl uoride exposure with cardiovascular diseases may be related to its ability to disturb lipid homeostasis, and trigger pro-infl ammatory cytokines and oxidative stress.

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Section: Il-6 = Interleukin-6; Tnf-α = Tumour Necrosis Factor-alpha; supporting

confidence: 94%

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Afolabi

Oyewo

Adekunle

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…Cell damage and cell death have been induced by the generation of ROS through the administration of a wide variety of chemical compounds, including fluoride (Varner et al, 1998). A close association between chronic fluoride toxicity and increased oxidative stress has been reported in humans (Jeji et al, 1985;Saralakumari and Ramakrishna, 1991;Li and Cao, 1994) and animals (Zhi-Zhong et al, 1989;Patel and Chinoy, 1998;Sharma and Chinoy, 1998). In one study, fluoride toxicity reduced certain intrinsic scavengers and resulted in increased oxygen free radical toxicity (Shivarajashankara et al, 2001).…”

Section: Discussionmentioning

confidence: 94%

“…Fluoride has been demonstrated in vivo and in vitro to cause increased lipid peroxidation in erythrocytes (Saralakumari and Ramakrishna, 1991), blood and some tissues (Zhi-Zhong et al, 1989;Patel and Chinoy, 1998;Sharma and Chinoy, 1998;Shivarajashankara et al, 2001). Oxidative stress produced by free radicals and H 2 O 2 is greater if fluoride impairs the production of free radical scavengers such as GSH-Px and SOD (Rzeuski et al, 1998).…”

Section: Discussionmentioning

confidence: 95%

Histopathological and biochemical changes in lung tissues of rats following administration of fluoride over several generations

Aydin

Çiçek

Akdoğan

et al. 2003

J of Applied Toxicology

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The possible effects of multigenerational administration of sodium fluoride (NaF) via drinking water on lung tissue morphology and biochemistry and body and lung weight were investigated in second-generation adult male rats. For this purpose we selected 45 Albino adult Wistar rats in nine cages, each of which consisted of four females and one male. Twenty-eight pregnant rats were selected for the experiment, divided into four groups of seven rats given 1 (control group), 10, 50 and 100 mg l(-1) NaF in drinking water during the gestation period. After gestation the rats had 165 pups in total. The mothers received fluoridated water during the lactation period and the offspring of the first generation had access to fluoridated water during the suckling period (21 days) and after the weaning period (30 days) until they became mature and at the start of the second part of the experiment. During this time 23 pups died and 79 female and 63 male first-generation rats survived. These first-generation rats were then used to obtain the second-generation offspring in the same manner as before, which were subjected to the same treatments. At the end of 6 months the rats were sacrificed and autopsied. Serum fluoride levels and the activities of principal antioxidant enzymes were determined in lung tissue samples taken from all groups. In addition, the lung tissues were submitted for histopathological examination. Histological findings showed alveolar congestion, alveolar cell hyperplasia and necrosis, prominent alveolar septal vessels, epithelial desquamation and macrophages in the alveolar spaces in the experimental groups. Additionally, there were inflammatory infiltrations in peribronchial, perivascular, intraparenchymal and respiratory tract lumen; intraparenchymal hyperaemic vessels; respiratory epithelial desquamation and proliferation; intraparenchymal thick walled vessels; parenchymal fibrosis; bronchiolitis; pneumonic and focal emphysematous areas. Furthermore, the lung parenchyma was observed to have a distorted appearance with loss of alveolar architecture. These histopathological findings were more pronounced for the rat groups of 50 and 100 mg l(-1) fluoride. No significant histopathological changes were observed in the rats of the control group. The increased activities of superoxide dismutase (SOD) and reduced glutathione peroxidase (GSH-Px) and the decreased activity of catalase (CAT) in the lung tissues with 10 mg l(-1) fluoride might indicate activation of the antioxidant defence mechanism. The decrease in SOD, GSH-Px and CAT activities with 50 and 100 mg l(-1) fluoride and the increase in thiobarbituric acid-reactive substance levels might be related to oxidative damage that occurred in the lung. This multigenerational evaluation of the long-term effect of different doses of fluoride intake through drinking water on lung damage shows that the lung tissues were damaged, there was emphysema and inflammation of lung parenchyma associated with loss of alveolar architecture and the degree of lung damage seemed to...

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“…A close connection between chronic fluoride toxicity and increased oxidative stress in both human (Saralakumari and Ramakrishna Rao, 1991;Jeji et al, 1985;Li and Cao, 1994) and animals (Zhi-Zhong et al,1989;Sharnia and Chinoy, 1998;Patel and Chinoy, 1998) have been reported. The ROS production is a natural process, and persistent high levels of ROS could damage the cell and its membrane.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of aqueous and ethanolic extracts of Tamarindusindica L. leaf on oxidative stress induced by sodium fluoride in different tissues of rat

Pandey¹,

Sar²,

Sinha³

et al. 2017

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The generation of reactive oxygen species (ROS) and lipid peroxidation has been considered to play an importa nt role in the pathogenesis of chronic fluoride toxicity. In the present study, the protective effects of aqueous and ethanolic extracts of tamarind leaf on fluoride induced oxidative stress in liver, kidney, heart and blood were studied. A total number of 36 female healthy albino rats were divided into six groups, each containing six animals. The control group (Gr-I) received normal drinking water and standard diet throughout the study period. The second group (Gr-II) received only 200 µg/ml (ppm) of sodium fluoride (NaF) in their drinking water for 60 days of study period. The third and fourth groups (Gr-III and Gr-IV) were co-administered with 200 ppm of NaF and low (200 mg /kg bwt) and high (300 mg/kg bwt) doses of ethanolic extract of tamarind leaf, respectively. While the fifth and sixth groups (Gr-V and Gr-VI) were similarly co-administered with 200 ppm of NaF in drinking water and low (200 mg /kg bwt) and high (300 mg/kg bwt) doses of aqueous extract of tamarind leaf, respectively for 60 days. Blood was collected at day 0, 30 and 60 of the study period. Liver, kidney and heart were obtained by sacrificing the rats for estimation of antioxidant parameters like super oxide dismutase (SOD), catalase, GSH (reduced glutathione) and (LP) lipid peroxidation. Gr-II showed significant reduction in the activity of catalase, SOD and GSH and significant increase in lipid peroxidation level of liver and kidney when compared with control group. In erythrocyte also, catalase, SOD, and GSH activity declined significantly and lipid peroxidation level increased at day 60 of experiment when compared with day 0. Heart tissue did not show any significant alteration in enzymatic activity. Among the leaf extracts at two different dose levels, aqueous extract at high dose (300 mg/kg bwt) showed better effect in protection of oxidative stress in liver, kidney, heart and erythrocytes of rat because status of oxidative stress which was almost negligible similar to the control group.

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Red blood cell glucose metabolism in human chronic fluoride toxicity

Cited by 23 publications

References 14 publications

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Histopathological and biochemical changes in lung tissues of rats following administration of fluoride over several generations

Protective effect of aqueous and ethanolic extracts of Tamarindusindica L. leaf on oxidative stress induced by sodium fluoride in different tissues of rat

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