Excess intake of fluoride for a prolonged period results in its accumulation predominantly in hard tissues, teeth and bones and causes diverse adverse effects that appear in the form of dental and skeletal fluorosis. Prolonged ingestion of fluoride also affects other organs and alters their architecture and physiology. Dental, skeletal and non-skeletal fluorosis have been described in different species of domestic animals due to excess concentration of fluoride in their drinking water, but maximum permissible or safe limit of fluoride in drinking water for these animals has not been well studied. Effects of different levels of fluoride exposures have been studied experimentally in laboratory animals, including rabbit, rat and mice. It has been found to affect digestive tract, liver, kidneys, brain, and endocrine organs, besides intrauterine development of foetus. But the exact mechanism involved in fluoride toxicity in these organs or tissues remain unanswered. Amelioration of fluorotoxicosis has been well observed in soft tissues in experimental study by using certain ameliorative agents such as ascorbic acid, vitamin A and D, calcium, boron, magnesium, and selenium compounds. Some herbal amelioration has also been investigated recently in sheep, goats and camels. This review provides comprehensive information on status of fluorosis in domestic and laboratory animals.

Status of Fluorosis in Animals

Dietary calcium supplementation reduces the bioavailability of fluoride from krill shell and NaF in rainbow trout (Oncorhynchus mykiss) reared in fresh water

Antarctic krill are a potential food source for humans and animals, but krill are known to contain high levels of fluorine(F). In this study, we investigated the toxicity of F in Antarctic krill using Wistar rats. There were three experimental groups: Thecontrol group were fed a basal diet, the krill treatment group were fed the same basal diet mixed with krill powder (150 mg·kg -1 F),and the sodium fluoride (NaF) treatment group were fed the basal diet with added NaF (150 mg·kg -1 F). General toxicity indicators including body weight and food intake were measured during the experiment. After three months the rats were dissected and tissue samples were collected from the liver, kidney, spleen, brain, and testis. Morphological changes in the cells of these tissues were assessed using HE staining. There were no significant differences in the body weight, the food intake, or the viscera coefficients among the three groups. In both treatment groups some pathological changes were observed in all soft tissue samples except thetestis, although there were fewer and less severe pathological changes in the krill treatment group than in the NaF treatment group.The results showed that the toxicity of F in Antarctic krill was lower than for an equivalent amount of F in NaF, but it was stilltoxic to rats consuming large quantities of krill. The findings of this study highlight the need for further investigation into potential F toxicity if krill is to be used for human consumption.

Evaluation of the toxicity of fluorine in Antarctic krill on soft tissues of Wistar rats

Antarctic krill is a potentially nutritious food source for humans, but fluorine (F) toxicity is a matter of concern. To evaluate the toxicity of F in Antarctic krill, 30 Wistar rats were divided into three groups with different dietary regimens: a control group, a krill treatment group (150 mg·kg -1 F), and a sodium fluoride (NaF) treatment group (150 mg·kg -1 F). After three months, F concentrations in feces, plasma, and bone were determined, and the degree of dental and skeletal fluorosis was assessed. The F concentrations in plasma and bone from the krill treatment group were 0.167 0±0.020 4 mg.L -1 and 2 709.8±301.9 mg·kg -1 , respectively, compared with 0.043 8±0.005 5 mg·L -1 and 442.4±60.7 mg·kg -1 , respectively, in samples from the control group. Concentrations of F in plasma and bone in the krill treatment group were higher than in the control group, but lower than in the NaF treatment group. The degree of dental fluorosis in the krill treatment group was moderate, compared with severe in the NaF treatment group and normal in the control group. The degree of skeletal fluorosis did not change significantly in any group. These results showed that the toxicity of F in Antarctic krill was lower than for an equivalent concentration of F in NaF, but it was toxic for rats consuming krill in large quantities. To conclude, we discuss possible reasons for the reduced toxicity of F in Antarctic krill. The present study provides a direct toxicological reference for the consideration of Antarctic krill for human consumption.

Evaluation of the biological toxicity of fluorine in Antarctic krill

Despite having an exceptionally high fluorine (F) concentration in their bones (up to 9000 μg/g in the present study), radiographs of mature Adélie penguins (Pygoscelis adeliae) do not show any symptoms of skeletal fluorosis. In this research, a series of chemical fractionation and speciation analyses for F gave a tentative explanation for this seemingly abnormal fact. The results showed that the inorganic fraction of F in penguin bones represented only about one-third of the total F with the rest bound organically, mostly in the form of fluorinated chitin or its derivatives. A laboratory experiment with rats on a high F intake indicated that chitin might prevent skeletal fluorosis by effectively combining with F and inhibiting abnormal mineralization, thereby decreasing the expected increase in bone mineral density.

Why do penguins not develop skeletal fluorosis

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Why do penguins not develop skeletal fluorosis