Flaxseed Oil (Linum usitatissimum) Prevents Cognitive and Motor Damage in Rats with Hyperammonemia.

Hyperammonemia is characterized by the excessive accumulation of ammonia in the body as a result of the loss of liver detoxification, leading to the development of hepatic encephalopathy (HE). These metabolic alterations carry cognitive and motor deficits and cause neuronal damage, with no effective treatment at present. In this study, we aimed to evaluate the effect of two subacute oral administrations of flaxseed oil (0.26 and 0.52 mL/kg) on short- and long-term memory, visuospatial memory, locomotor activity, motor coordination, and the neuronal morphology of the prefrontal cortex (PFC) via tests on Wistar rats with hyperammonemia. The goal was to identify its role in the regulation of cerebral edema, without liver damage causing cerebral failure. In contrast with an ammonium-rich diet, flaxseed oil and normal foods did not cause cognitive impairment or motor alterations, as evidenced in the short-term and visuospatial memory tests. Furthermore, the flaxseed oil treatment maintained a regular neuronal morphology of the prefrontal cortex, which represents a neuroprotective effect. We conclude that the oral administration of flaxseed oil prevents cognitive and motor impairments as well as neuronal alterations in rats with hyperammonemia, which supports the potential use of this oil to ameliorate the changes that occur in hepatic encephalopathy.

[Osteoporosis treatment evaluation with desoxypiridinoline urine detection in postmenopause patients]. / Evaluación del tratamiento de osteoporosis con determinación urinaria de desoxipiridinolina en mujeres posmenopáusicas.

OBJECTIVE: to evaluate urinary desoxypiridinoline (Dpd) levels in postmenopause patients, with osteoporosis or osteopenia after treatment with sodium alendronate. METHODS: a quasiexperimental study was carried out in 118 patients, aged from 41 to 69 years. According to the densitometry results and treatment received, we formed five groups: group I, patients with osteoporosis, treated with 10 mg/day of alendronate; group IIA, patients with osteopenia treated with alendronate 5 mg/day; group IIB, patients with osteopenia treated with hormonal therapy replacement (HTR); group IIIA, patients with normal densitometry treated with change of life style habits; and group IIIB, patients with normal densitometry treated with HTR. Dpd urinary levels were measured in all patients at the beginning and 60 days after. The statistical analysis was t Student paired. RESULTS: the group I diminished 7.8 nmol Dpd/mmol Cr with a p = 0.001. In the other groups the reduction of the urinary Dpd level was not significant. CONCLUSIONS: in osteoporosis the urinary Dpd excretion diminishes after 60 days of treatment with 10 mg/day of sodium alendronate.