1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Objectives: Odontogenic cysts and tumors are the most relevant lesions that affect the gnathic bones. These lesions have in common the formation of cystic areas and this common feature may suggest involvement of similar mechanisms. The hypoxia inducible factor 1 alpha (HIFa responsive protein to hypoxia and caspase-3, an irreversible apoptosis marker, may contribute to cyst formation. Thus, this study aimed to investigate the immunoexpression of these proteins in odontogenic cysts and tumors. Material and methods: Twenty cases of ameloblastoma, keratocystic odontogenic tumor (KOT) (n=20), radicular cyst (RC) (n=18), dentigerous cyst (DC) (n=11), calcifying cystic odontogenic tumor (n=8) and dental follicle (DF) (n=10) were used to investigate HIF-and caspase-3 expression in sequential serial cuts by immunohistochemistry. Results: HIF-was overexpressed in RC, DC and ameloblastoma when compared with DF. The basal and sometimes the lower suprabasal layer showed no or very low expression in DC, KOT and ameloblastoma, the last also showing strong expression in solid epithelial areas and initial cystic formation regions. Caspase-3 was found to be overexpressed in all lesions, with the highest expression in odontogenic cysts compared to tumors. HIF-and caspase-3 were localized in similar areas of the same lesions, especially in the epithelium surrounding cystic formations. Conclusions: This study showed distinct immunoexpression of HIF-and caspase-3 in odontogenic cyst and tumors, with higher expression observed in odontogenic cysts. Clinical relevance: These finding suggesting a possible correlation between hypoxia, apoptosis and cystogenesis, leading to understand the mechanisms responsible to cystic formation in odontogenic lesions.

The aims of this study were to evaluate whether chronic intoxication with mercury chloride (HgCl2), in a low concentration over a long time, can be deposited in the central nervous tissue and to determine if this exposure induces motor and cognitive impairments. Twenty animals were intoxicated for 45 days at a dose of 0.375 mg/kg/day. After this period, the animals underwent a battery of behavioral tests, in a sequence of open field, social recognition, elevated T maze and rotarod tests. They were then sacrificed, their brains collected and the motor cortex and hippocampus dissected for quantification of mercury deposited. This study demonstrates that long-term chronic HgCl2 intoxication in rats promotes functional damage. Exposure to HgCl2 induced anxiety-related responses, short- and long-term memory impairments and motor deficits. Additionally, HgCl2 accumulated in both the hippocampus and cortex of the brain with a higher affinity for the cortex.

AME showed an increased presence of proteins associated with tumour invasiveness, which indicates a possible role of these proteins in the biological behaviour of this tumour.

Mercury exposure is considered to be a public health problem due to the generation of toxic effects on human health as a result of environmental and occupational conditions. The inorganic form of mercury (HgCl) can cause several biological changes in cells and tissues through its cumulative toxic potential, but little has been experimentally proven about the effects of inorganic mercury on salivary glands, an important modulator organ of oral health. This study analyzes the effects of prolonged low dose exposure to HgCl on the salivary glands of rats. Adult animals received a dose of 0.375 mg kg day over a period of 45 days. The parotid and submandibular glands were collected for analysis of the mercury levels and evaluation of oxidative stress, histological parameters and immunomodulation for metallothionein I and II (MT-I/II). In this investigation, biochemical and tissue changes in the salivary glands were verified due to the mercury levels, causing reduction in antioxidant capacity against peroxyl radicals, with consequent cellular lipid peroxidation and an increase in nitrite levels, volumetric changes and cytoskeletal damage in the submandibular glands, with less severe damage to the parotid glands. The results also have shown the occurrence of a cytoprotection mechanism due to increased MT-I/II expression, but not enough to avoid the morphology and oxidative damage. This evidence highlights, for the first time, that inorganic mercury is able to alter the morphology and oxidative biochemistry in salivary glands when exposed for a long time in low doses.