Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain

Banala, Rajkiran Reddy; Karnati, Pratap Reddy

doi:10.1016/j.ijdevneu.2015.08.010

Cited by 32 publications

(35 citation statements)

References 36 publications

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“…Moreover, increased intensity of oxidation of lipids and proteins was observed in the cerebral cortex, cerebellum and medulla oblongata (the concentration of fluorine in drinking water, 50 and 150 mg/L). These results were confirmed by another analysis in which, among rats exposed to fluorine in the prenatal and postnatal periods, increased concentrations of fluorine in the serum and the brain were observed as early as on the 14th day of life, which resulted in the decreased activity of SOD and higher intensity of lipid peroxidation in the brains of the analysed animals (the concentration of fluorine in drinking water, 20 mg/L) [33, 42]. An increase in the concentration of the products of lipid oxidation was also observed among adult rats that were exposed to 10 mg/L of fluorine concentration in drinking water.…”

Section: Introductionmentioning

confidence: 54%

“…Among both young and adult specimens exposed to the toxic influence of high doses of fluorine, we can observe impaired ability to learn, disturbances in memory and information processing and behavioural problems. All of these cause a decrease in the quality of life [42]. Numerous reports concerning the occurrence of endemic fluorosis lead to the establishment of an accepted concentration of fluorine in drinking water by the World Health Organization (WHO) at a level of which the element does not accumulate excessively in the human organism and does not cause adverse effects.…”

Section: Introductionmentioning

confidence: 99%

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The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Dec

Łukomska

Maciejewska

et al. 2016

Biol Trace Elem Res

124

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Fluorides occur naturally in the environment, the daily exposure of human organism to fluorine mainly depends on the intake of this element with drinking water and it is connected with the geographical region. In some countries, we can observe the endemic fluorosis—the damage of hard and soft tissues caused by the excessive intake of fluorine. Recent studies showed that fluorine is toxic to the central nervous system (CNS). There are several known mechanisms which lead to structural brain damage caused by the excessive intake of fluorine. This element is able to cross the blood-brain barrier, and it accumulates in neurons affecting cytological changes, cell activity and ion transport (e.g. chlorine transport). Additionally, fluorine changes the concentration of non-enzymatic advanced glycation end products (AGEs), the metabolism of neurotransmitters (influencing mainly glutamatergic neurotransmission) and the energy metabolism of neurons by the impaired glucose transporter—GLUT1. It can also change activity and lead to dysfunction of important proteins which are part of the respiratory chain. Fluorine also affects oxidative stress, glial activation and inflammation in the CNS which leads to neurodegeneration. All of those changes lead to abnormal cell differentiation and the activation of apoptosis through the changes in the expression of neural cell adhesion molecules (NCAM), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and MAP kinases. Excessive exposure to this element can cause harmful effects such as permanent damage of all brain structures, impaired learning ability, memory dysfunction and behavioural problems. This paper provides an overview of the fluoride neurotoxicity in juveniles and adults.

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Section: Introductionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Dec

Łukomska

Maciejewska

et al. 2016

Biol Trace Elem Res

124

View full text Add to dashboard Cite

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“…Vitamin A (retinol) is one of the fat‐soluble vitamins, works as a antioxidative agent as it neutralizes the free radicals (Banala & Karnati, ; Li, Li, Chen, & Chen, ). Li et al.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin A (retinol) is one of the fat-soluble vitamins, works as a antioxidative agent as it neutralizes the free radicals (Banala & Karnati, 2015;Li, Li, Chen, & Chen, 2016). Li et al (2016) determined that VA status and its metabolism in the fasting and refeeding cycles contribute to the regulation of the expression of genes in hepatic glucose and lipid metabolism in rats.…”

Section: Discussionmentioning

confidence: 99%

The effects on some non-enzymatic antioxidants and oxidative stress ofAstacus leptodactylus(Esch., 1823) of starvation periods

Barim‐Oz

2017

Aquacult Nutr

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This study investigated the effect of starvation (78 days) and refeeding (33 days) on the oxidative stress [malondialdehyde (MDA)] and the non‐enzymatic antioxidants [vitamin E (VE), vitamin C (VC), vitamin A (VA), beta carotene (βC) and reduced glutathione (GSH)] in the hepatopancreas, muscle and gill tissues of freshwater crayfish (Astacus leptodactylus). Crayfish were divided into three experimental groups: control (fed), starved (not fed) crayfish for 78 days and refeeding crayfish for 33 days after 78 days of starvation. The biochemical analysis of the tissues was conducted at 3, 18, 33, 48, 63 and 78 days of starvation and feeding and at 3, 18 and 33 days of refeeding. It was determined that crayfish can withstand starvation period of 78 days. In all of the periods, the MDA levels were significantly higher in the tissues of starved crayfish when compared with the control. The findings of this study demonstrate that starvation has a negative effect on the VE, VC, VA, βC and GSH levels in the crayfish. The measured parameters returned to control values after 33 days of the refeeding. Additionally, the starvation resulted in decreased levels of VE, VA and βC in the abdomen muscle of crayfish consumed by humans.

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“…Earlier reports on natural products which aid in protection against NaF induced behavioral alterations are: Curcumin 17 , Quercetin 18 , Rutin (extracted compound of Okra) 19 , Vitamin A 20 , and Spirulina platensis 21 . These natural products reverse behavioral alterations which are induced on NaF exposure.…”

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confidence: 99%

Untitled

2018

IJPSR

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This study reports protective effect of Abelmoschus moschatus seed extract against sodium fluoride (NaF) induced alterations in behavior correlated with neurochemical changes in developing brain of rats. Excessive intake of fluoride during pregnancy cross the blood brain barrier (BBB) and cause adverse effects on neonatal development. As the BBB in fetuses, neonates and infants is immature, it cannot provide protection against the entries. The pregnant wistar rats were randomly categorized into six groups of five animals each. Group I is of control rats received normal tap water. Group II is NaF exposed group with 20 ppm (or 20 mgkg -1 body wt.) in their drinking water. Group III rats were treated with A. moschatus aqueous extract (AMAE) (300 mgkg -1 body wt./day/rat) along with NaF water (20 ppm). Group IV rats were treated with A. moschatus ethanolic extract (AMEE) (300 mgkg -1 body wt./day/rat) along with NaF water (20 ppm).Group V and VI rats were treated with AMAE (300 mgkg -1 body wt./day/rat), and AMEE (300 mgkg -1 body wt./day/rat) respectively. On 1 st , 7 th , 14 th , 21 st and 30 th day (postpartum days), the pups were sacrificed to assess oxidative stress markers (LPO, CAT), and measured body weight, brain weight, BSI, and estimated protein content of brain tissue of all experimental groups. On post-natal day 21 and day 30 pups behavioral activity (rota rod, hot plate test) was measured. Fluoride exposure significantly increased lipid peroxidation and decreased the activity of catalase, and decreased body and brain weight, BSI and also protein content of the brain of pups indicating oxidative stress and inhibited antioxidant system and protein synthesis which were reverted on administration of AMAE and AMEE against NaF intoxication. The altered behavioral responses on NaF exposure were also reversed to that of control. Hence, this study proves the vulnerability of developing brain to fluoride toxicity during development and growth and protection offered by AMAE and AMEE towards neurotoxicity of NaF.

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Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain

Cited by 32 publications

References 36 publications

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

The effects on some non-enzymatic antioxidants and oxidative stress ofAstacus leptodactylus(Esch., 1823) of starvation periods

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