The aim of this study was to examine the relationship between the L55M and Q192R paraoxonase (PON1) polymorphisms and obesity in a population of adult Mexican workers. The study population included 127 adult individuals from the Universidad Autónoma del Estado de Morelos, ranging in age from 20 to 56 years and representing both sexes. Based on body mass index, 63 individuals were classified as obese and 64 as normal weight. The PON1-Q192R and PON1-L55M polymorphisms were determined by restriction fragment length polymorphism PCR analysis. Both arylesterase and paraoxonase activity levels were similar in both groups, whereas systolic pressure, triglyceride, total cholesterol, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, glucose, and insulin levels were higher in the obese group than in the normal-weight group (P < 0.05). An exception was the high-density lipoprotein cholesterol (HDL-C) levels, which were lower in the obese group (P < 0.05). Although the PON1-Q192R polymorphism was not associated with either group, the frequency of the homozygous L genotype for the PON1-L55M polymorphism was higher in the obese group than in the normal-weight group (P < 0.05). In conclusion, this study established a positive association between the PON1-L55M homozygous L genotype and obesity.

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In the present work we established a relationship between some physicochemical properties of two different batches of Prussian blue (PB) and their in vivo efficacy as an antidote against thallium poisoning. The physicochemical properties studied were crystallite size and thallium-adsorbing capacity. One of the batches was synthesized and the other was obtained from commercial sources. The synthesized PB batch with the smallest crystallite size had both the highest adsorption capacity and antidotal efficacy. Synthesized PB protected 100% of the animals against one LD50 thallium dose, whereas the commercial PB batch protected only 80%. Thallium content in blood and tissues (liver, kidney, brain) was also analysed after antidotal PB treatment in rats previously intoxicated with a sublethal dose of T1+. Animals treated with synthesized PB showed significantly less thallium in blood and tissue contents than those values of commercial PB-treated rats, indicating better antidotal properties of the synthesized PB. According to the present study we suggest an in vivo evaluation of the compound before distribution of the product to toxicological units, if X-ray diffractometric analysis is not available, in order to identify and determine the crystallite size of the compound as it plays an important role in the efficacy of PB.

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by the irreversible loss of dopaminergic neurons in the nigrostriatal pathway with subsequent dopamine deficiency. Environmental causes have been proposed through molecules, such as 1-methyl-4-phenylpyridinium (MPP(+)), to induce oxidative stress. The methanolic extract of plants of the genus Buddleja has been reported to have in vitro and in vivo antioxidant properties to protect against neuronal death. In the present study, the neuroprotective effect of Buddleja cordata methanolic extract in the MPP(+) PD rat model was investigated. Animals were administered orally with 50 or 100 mg/kg of methanolic extract every 24 h for 14 days. Twenty hours later, rats were infused with an intrastriatal stereotaxic microinjection of 10 µg MPP(+) in 8 μl sterile saline solution. Six days later, the animals were treated with 1 mg/kg apomorphine to record ipsilateral rotations for 1 h. All the rats were killed by decapitation and the lesioned striatum was dissected for dopamine and lipid peroxidation quantifications. Both methanolic extract doses led to a significantly lower (P < 0.05) number of ipsilateral rotations (75-80 %). This behavioral protection was corroborated with 60 % level of dopamine preservation (P < 0.05) and 90 % decrease in the formation of lipidic fluorescent products in the striatum (P < 0.05). This study demonstrates the antioxidant and neuroprotective effect of Buddleja cordata methanolic extract in the MPP(+) PD rat model, possibly due to the involvement of phenylpropanoids.

EGb761 produces reversible inhibition of both monoamine oxidase (MAO) isoforms in the central nervous system. 1-Methyl-4-phenylpyridinium (MPP+) neurotoxicity is prevented by treatment with the MAO inhibitor pargyline. We investigated EGb761's effect on striatal MAO activity during MPP+ neurotoxicity. C-57 black mice were pretreated with EGb761 (10 mg/kg) daily for 17 days followed by administration of MPP+ (0.72 mg/kg). MPP+ enhanced striatal MAO (30%) activity at 6 h, and EGb761 prevented this effect. MAO-B activity in striatum was enhanced (70%) 6 h after MPP+ administration and was reduced to almost normal levels in EGb761 + MPP+ group compared to MPP+ group. Pretreatment with EGb761 partially prevented (32%) the striatal dopamine-depleting effect of MPP+ and prevented the reduction in striatal tyrosine hydroxylase activity (100%). Results suggest that EGb761 supplements may be effective in reducing MAO activity as well as enhancement in dopamine metabolism, thereby preventing MPP+-neurotoxicity.

After transient cerebral ischemia and reperfusion (I/R), damaging mechanisms, such as excitotoxicity and oxidative stress, lead to irreversible neurological deficits. The induction of metallothionein-II (MT-II) protein is an endogenous mechanism after I/R. Our aim was to evaluate the neuroprotective effect of MT-II after I/R in rats. Male Wistar rats were transiently occluded at the middle cerebral artery for 2 h, followed by reperfusion. Rats received either MT (10 μg per rat i.p.) or vehicle after ischemia. Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; also, neurological deficit was evaluated after ischemia, using the Longa scoring scale. Infarction area was analyzed 72 hours after ischemia. Results showed increased LP in frontal cortex (30.7%) and hippocampus (26.4%), as compared to control group; this effect was fully reversed by MT treatment. Likewise, we also observed a diminished neurological deficit assessed by the Longa scale in those animals treated with MT compared to control group values. The MT-treated group showed a significant (P < 0.05) reduction of 39.9% in the infarction area, only at the level of hippocampus, as compared to control group. Results suggest that MT-II may be a novel neuroprotective treatment to prevent ischemia injury.

This study found that leptin was associated with the MetS, especially in obesity and insulin resistance, indicating a high risk for university workers to develop hypertension, DM2, and cardiovascular disease.