Abstract
In our experiment, the 1-month effects of caffeine (Caff) and fluoride (F) administered separately and together on nitric oxide and total antioxidant status in serum, brain, liver and kidney of rats were investigated. Also, the influence of caffeine on fluoride excretion with urine was studied. Thirty adult male Wistar rats were divided into five equal groups of six each: (I) controls drinking tap water; (II) controls drinking tap water and receiving intragastrically 0.5 ml of tap water; (III) animals receiving 25 mg F/L in drinking water; (IV) animals receiving 4.7 mg Caff/kg bw/day; (V) animals receiving 25 mg F/L in drinking water and 4.7 mg Caff/kg bw/day. The applied fluoride caused increase of nitric oxide level (NO), intensified lipid peroxidation (TBARS) and decreased total antioxidant status in serum (TAS), brain, kidney and liver. Caffeine administered intragastrically, as an antioxidant, was relatively efficient in alleviating these adverse effects of F. In rats treated only with fluoride the F excretion in urine significantly increased in an exposure-time dependent-manner and did not change both in rats treated with Caff and co-exposed to Caff and F.
-
-
Protective effects of blackberry and quercetin on sodium fluoride-induced oxidative stress and histological changes in the hepatic, renal, testis and brain tissue of male rat
BACKGROUND: Sodium fluoride (NaF) intoxication is associated with oxidative stress and altered antioxidant defense mechanism. The present study was carried out to evaluate the potential protective role of blackberry and quercetin (Q) against NaF-induced oxidative stress and histological changes in liver, kidney, testis and brain tissues of rats. METHODS: The rats
-
Conceivable amelioration of NaF-induced toxicity in liver, kidney and brain of chicken by black tea extract: an in vitro study.
Sodium fluoride (NaF) toxicity on enzymatic and non-enzymatic oxidative stress markers of chicken liver, kidney and brain homogenate in in vitro condition where studied in present investigation. We studied alteration in the activity of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO) and glutathione (GSH) content to study oxidative stress.
-
Evaluation of free radical-scavenging and anti-oxidant properties of black berry against fluoride toxicity in rats
Oxidative damage to cellular components such as lipids and cell membranes by free radicals and other reactive oxygen species is believed to be associated with the development of degenerative diseases. Fluoride intoxication is associated with oxidative stress and altered anti-oxidant defense mechanism. So the present study was extended to investigate
-
A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
-
Effects of individual and combined exposure to sodium arsenite and sodium fluoride on tissue oxidative stress, arsenic and fluoride levels in male mice.
Arsenic and fluoride are potent toxicants, widely distributed through drinking water and food and often result in adverse health effects. The present study examined the effects of sodium meta-arsenite (100 mg/l in drinking water) and sodium fluoride (5 mg/kg, oral, once daily), administered either alone or in combination for 8
Related Studies :
-
-
-
Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
-
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,
-
NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
-
Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
-
Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
Related FAN Content :
-