Effects of long-term fluoride exposure are associated with oxidative biochemistry impairment and global proteomic modulation, but not genotoxicity, in parotid glands of mice.

BACKGROUND: Fluoride has become widely used in dentistry because of its effectiveness in caries control. However, evidence indicates that excessive intake interferes with the metabolic processes of different tissues. Thus, this study aimed to investigate the effects of long-term exposure to F on the parotid salivary gland of mice, from the analysis of oxidative, proteomic and genotoxic parameters. MATERIALS AND METHODS: The animals received deionized water containing 0, 10 or 50 mg/L of F, as sodium fluoride, for 60 days. After, parotid glands were collected for analysis of oxidative biochemistry, global proteomic profile, genotoxicity assessment and histopathological analyses. RESULTS: The results revealed that exposure to fluoride interfered in the biochemical homeostasis of the parotid gland, with increased levels of thiobarbituric acid reactive species and reduced glutathione in the exposed groups; as well as promoted alteration of the glandular proteomic profile in these groups, especially in structural proteins and proteins related to oxidative stress. However, genotoxic assessment demonstrated that exposure to fluoride did not interfere with DNA integrity in these concentrations and durations of exposure. Also, it was not observed histopathological alterations in parotid gland. CONCLUSIONS: Thus, our results suggest that long-term exposure to fluoride promoted modulation of the proteomic and biochemical profile in the parotid glands, without inducing damage to the genetic component. These findings reinforce the importance of rationalizing the use of fluorides to maximize their preventative effects while minimizing the environmental risks.

Early biochemical biomarkers for zinc in silver catfish (Rhamdia quelen) after acute exposure.

Contamination of aquatic ecosystems by metals causes various biochemical changes in aquatic organisms, and fish are recognized as indicators of environmental quality. Silver catfish were exposed to six concentrations of zinc (Zn): 1.0, 2.5, 5.0, 7.5, 10.0 and 12.5 mg/L for 96 h to determine the mean lethal concentration (LC50). The value obtained was 8.07 mg/L. In a second experiment, fish were exposed to concentrations of 1.0 or 5.0 mg/L Zn and a control for 96 h. Afterward, the tissues were collected for biochemical analysis. Lipid peroxidation, as indicated by thiobarbituric acid-reactive substance (TBARS), decreased in the liver and brain for all Zn concentrations tested, while in the gills TBARS levels increased at 1.0 mg/L and declined at 5.0 mg/L. Zn increased protein carbonyls in the muscle of silver catfish and decreased it in the other tissues. The enzyme superoxide dismutase increased in both exposed groups. However, catalase did not change. Glutathione S-transferase decreased in the liver and increased in the gills (1.0 mg/L), muscle (5.0 mg/L) and brain (1.0 and 5.0 mg/L). Nonprotein thiols changed only in brain and muscle tissue. Zn exposure inhibited acetylcholinesterase (AChE) activity in the brain at both concentrations tested, but did not change it in muscle. Exposure to Zn inhibited the activity of Na(+)/K(+)-ATPase in the gills and intestine at both concentrations tested. Our results demonstrate that Zn alters biochemical parameters in silver catfish and that some parameters such as AChE and Na(+)/K(+)-ATPase could be considered as early biomarkers of waterborne Zn toxicity.