Effects of Chronic Ethanol Consumption and Ovariectomy on the Spontaneous Alveolar Bone Loss in Rats.

Postmenopausal estrogen deficiency and ethanol (EtOH) abuse are known risk factors for different diseases including bone tissues. However, little is known about the synergic effects of EtOH abuse and estrogen deficiency on alveolar bone loss in women. The present study evaluated the effects of EtOH chronic exposure and ovariectomy on the alveolar bone loss in female rats. For this, 40 female Wistar rats were randomly divided into 4 groups: control, EtOH exposure, ovariectomy (OVX), and OVX plus EtOH exposure. Initially, half of the animals were ovariectomized at 75 days of age. After that, the groups received distilled water or EtOH 6.5 g/kg/day (20% w/v) for 55 days via gavage. Thereafter, animals were sacrificed and the mandibles were collected, dissected, and separated into hemimandibles. Alveolar bone loss was evaluated by measuring the distance between the cementoenamel junction and the alveolar bone crest through a stereomicroscope in 3 different anatomical regions of the tissue. One-way ANOVA and post hoc Tukey were used to compare groups (p < 0.05). The results showed that the ovariectomy and EtOH exposure per se were able to induce alveolar bone loss, and their association did intensify significantly the effect. Therefore, OVX associated with heavy EtOH exposure increase the spontaneous alveolar bone loss in rats.

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies.

Stroke is a leading cause of death and neurological disability worldwide and striatal ischemic stroke is frequent in humans due to obstruction of middle cerebral artery. Several pathological events underlie damage progression and a comprehensive description of the pathological features following experimental stroke in both acute and chronic survival times is a necessary step for further functional studies. Here, we explored the patterns of microglial activation, astrocytosis, oligodendrocyte damage, myelin impairment, and Nogo-A immunoreactivity between 3 and 30 postlesion days (PLDs) after experimental striatal stroke in adult rats induced by microinjections of endothelin-1 (ET-1). The focal ischemia induced tissue loss concomitant with intense microglia activation between 3 and 14 PLDs (maximum at 7 PLDs), decreasing afterward. Astrocytosis was maximum around 7 PLDs. Oligodendrocyte damage and Nogo-A upregulation were higher at 3 PLDs. Myelin impairment was maximum between 7 and 14 PLDs. Nogo-A expression was higher in the first week in comparison to control. The results add important histopathological features of ET-1 induced stroke in subacute and chronic survival times. In addition, the establishment of the temporal evolution of these neuropathological events is an important step for future studies seeking suitable neuroprotective drugs targeting neuroinflammation and white matter damage.

Evaluation of the effects of chronic intoxication with inorganic mercury on memory and motor control in rats.

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.