The isoflavones mixture from Trifolium pratense L. protects HCN 1-A neurons from oxidative stress

Oxidative stress-induced neuronal cell death has been implicated in different neurological disorders and neurodegenerative diseases such as Alzheimer's disease and Parkinson's. Using the Alzheimer's disease-associated hydrogen peroxide (H(2)O(2)), we investigated the neuroprotective efficacy of a natural mixture of phytoestrogenic isoflavones (genistein, daidzein, biochanin A and formononetin) from Trifolium pratense L. (Red clover) against oxidative stress-induced cell death in human cortical cell line HCN 1-A maintained in culture. Neuronal viability was determined by MTT or trypan blue test and neuronal integrity by morphological analysis.The results obtained indicate that exposure of HCN 1-A cell cultures to hydrogen peroxide resulted in a concentration-dependent decrease in neuron viability. Concentration of H(2)O(2) ranging from 50 to 200 microg/ml were toxic to these cultures. A 24-hour pretreatment with 0.5, 1 and 2 microg/ml isoflavones extract significantly increased cell survival as evidenced by MTT or trypan blue test and significantly prevented the morphological disruption caused by H(2)O(2) as shown by microscopical inspection, indicating that neurons treated with isoflavones were protected from the cell death induced by H(2)O(2) exposure. These findings imply that the neuroprotective effect of isoflavones extract is partly associated with its antioxidant activity. Further, results of these investigations indicate that although isoflavones extract exert a neuroprotective effect, it do not promoted cortical neuron process outgrowth.     

Vitamin E deficiency secondary to chronic intestinal malabsorption and effect of vitamin supplement: a case report.

We report the clinical, neurophysiological (comprehending electromyography, nerve conduction velocities, and multimodal evoked potentials), histological study of the nerve and muscle and the effect of vitamin E supplement in a 32-year-old case with chronic vitamin E deficiency subsequent to acquired intestinal malabsorption. An early diagnosis for an early treatment is essential in preventing severe neurological deterioration.     

Variations in ferritin levels in blood during physiological pregnancy

Iron deficiency anemia is the most frequent haematological pathology in pregnancy. Serum ferritin levels represent the state of iron deposits. Low levels are a sure sign of iron deficiency. At the University of Turin we studied the variations of serum ferritin levels during physiological pregnancy and the sensitivity of routine blood tests with respect to serum ferritin levels. Routine haematological blood values along with ferritin levels were measured in 115 patients throughout pregnancy. The mean serum ferritin level was 56 ng/ml in the first trimester, 27.2 ng/ml in the second and 11.8 ng/ml in the third. The incidences of anemia per trimester was 6.6%, 4.8% and 49% respectively (p less than 0.05, chi squared). Our results show that it is important to evaluate iron deposits early in pregnancy by measuring serum ferritin levels in order to determine the need for iron therapy.     

Reduced ACTH/cortisol responses to naloxone in men with Parkinson's disease

Summary In order to establish whether the inhibitory control exerted by endogenous opioid peptides on ACTH/cortisol secretion changes in patients affected by Parkinson's disease, ten parkinsonian male subjects and eight age matched normal controls were tested with naloxone (4 mg an i.v. bolus plus 10 mg infused in two hours). In a different occasion all subjects were tested with normal saline. Experiments started at 09.00 h. Plasma ACTH and cortisol concentrations showed a slight physiological decline during saline test in both groups. In the normal controls and in the parkinsonian patients both ACTH and cortisol levels were significantly higher after naloxone administration than during saline test. However, both naloxone induced ACTH and cortisol responses were significantly higher in normal than in parkinsonian subjects. In agreement with the well-known opioid deficiency characterizing the parkinsonian brain, these data show a reduced opioid inhibitory control of ACTH/cortisol secretion in patients with Parkinson's disease.     

Reduction of GH response to the GABA-B agonist baclofen in patients with major depression

In order to establish whether alterations in the GABAergic control of GH secretion occur in male patients with major depression, the GH response to the GABAergic-B agonist baclofen (10 mg at 0830h) or to placebo was tested in 9 depressed men and in 10 age- and weight-matched male normal controls.

The basal concentrations of GH were significantly lower in the depressed patients (0.87± 0.69 ng/ml) than in the normal controls (1.57±0.33 ng/ml) (p=0.011) and were not modified by the administration of placebo. The administration of baclofen induced a striking, significant increase in GH concentrations in the normal controls (mean peak at 90 MIN=6.4±1.5 ng/ml). In contrast, a slight, nonsignificant GH increase occurred in the depressed patients after baclofen (mean peak at 90 MIN=1.57±1.45 ng/ml). The GH response was significantly lower in the depressed than in the control subjects (p<0.001). These data indicate the presence of reduced GABAergic control of GH secretion in male depressed patients.