Abstract
The study evaluated the effect of commercial preparation of deltamethrin, Butox®, and fluoride (F–) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox®, providing deltamethrin at the dose rate of 1.28?mg per kg body weight per day. Group C was administered F–, as NaF, in drinking water providing 20?ppm F–. Group D received both deltamethrin and F– at the same dosages as groups B and C, respectively. Although, glutathione S-transferase activity was induced only in Butox® alone treated group, the activities of superoxide dismutase and catalase were inhibited in all treatment groups when compared to the control group. Elevated lipid peroxidation was observed in the groups exposed to F–. The activity of erythrocyte acetylcholinesterase (AChE) was inhibited in Butox® treated groups, whereas brain AChE activity was inhibited in all treatment groups. In conclusion, both deltamethrin (given as Butox®) and F– inhibit AChE activity and produce oxidative stress in brain with F– producing more oxidative damage. However, compared to the individual exposures, the co-exposure of these chemicals does not produce any exacerbated alteration in these biochemical parameters.
-
-
Combination of fluoride and endosulfan induced teratogenicity and developmental toxicity in Swiss albino mice exposed during organogenesis.
The present investigation was conducted to evaluate the teratogenic and developmental toxicity of fluoride and endosulfan alone and in combination in pregnant Swiss albino mice exposed during the organogenetic period (5-14 days) of gestation. Fluoride (25.1 mg/kg body weight in water) and endosulfan (1.8 mg/kg bw by oral intubation) when
-
[Biological exposure limits caused by co exposure to fluoride and arsenic based on Wnt signaling pathway].
Chronic fluoride-arsenic combined poisoning is a global public health problem. While the cause of the disease is clear, the pathogenesis is unknown. Given that there is no specific treatment, early prevention is particularly important. Biological exposure limits are designed to investigate the maximum allowable concentration of harmful effects from exogenous
-
Interplay of ROS and behavioral pattern in fluoride exposed Drosophila melanogaster.
Highlights NaF exposure increases mortality and changes male-female ratio in Drosophila. NaF treatment alters the activities endogenous antioxidant enzymes. Chronic sub-lethal NaF exposure causes increased oxidative damage. NaF decreases brain cell viability and increases DNA damage. NaF exposure alters selected behavioral pattern in Drosophila melanogaster. Reactive oxygen species (ROS) is
-
A correlation between serum vitamin, acetylcholinesterase activity and IQ in children with excessive endemic fluoride exposure in Rajasthan, India
Fluoride is widely distributed in nature and a direct source of adverse health effects in human populations. Fluoride poisoning attributed by long-term exposure to high levels of fluoride [is] called fluorosis. The present study was carried out among 9-14 years old school children of Dausa district, Rajasthan India. The subjects
-
Effects of high fluoride and arsenic on brain biochemical indexes and learning-memory in rats
Nine-six Wistar rats were randomly divided into four groups of 24 rats in each group (female:male = 1:1). Over a period up to 90 days, with one untreated group as controls, the other three groups were administered, respectively, high fluoride (100 mg NaF/L), high arsenic (50 mg As2O3/L), or both
Related Studies :
-
-
-
Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
-
Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
-
Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
-
Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
-
Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
Related FAN Content :
-