Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters











Database
Language
Publication year range
1.
Physiol Behav ; 173: 200-208, 2017 05 01.
Article in English | MEDLINE | ID: mdl-28209536

ABSTRACT

Melatonin is a radical scavenger with the ability to remove reactive oxidant species. There is report that co-exposure to lead and ethanol during developmental stages induces learning and memory deficits and oxidative stress. Here, we studied the effect of melatonin, with strong antioxidant properties, on memory deficits induced by lead and ethanol co-exposure and oxidative stress in hippocampus. Pregnant rats in lead and ethanol co-exposure group received lead acetate of 0.2% in distilled drinking water and ethanol (4g/kg) by oral gavages once daily from the 5th day of gestation until weaning. Rats received 10mg/kg melatonin by oral gavages. On postnatal days (PD) 30, rats trained with six trials per day for 6 consecutive days in the water maze. On day 37, a probe test was done and oxidative stress markers in the hippocampus were evaluated. Results demonstrated lead and ethanol co-exposed rats exhibited higher escape latency during training trials and reduced time spent in target quadrant, higher escape location latency in probe trial test and had significantly higher malondialdehyde (MDA) levels, significantly lower superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities in the hippocampus. Melatonin treatment could improve memory deficits, antioxidants activity and reduced MDA levels in the hippocampus. We conclude, co-exposure to lead and ethanol impair memory and melatonin can prevent from it by oxidative stress modulation.


Subject(s)
Antioxidants/administration & dosage , Ethanol/toxicity , Lead/toxicity , Maternal Exposure , Melatonin/administration & dosage , Memory Disorders/chemically induced , Memory Disorders/prevention & control , Age Factors , Analysis of Variance , Animals , Animals, Newborn , Catalase/metabolism , Drug Administration Schedule , Female , Glutathione Peroxidase/metabolism , Hippocampus/drug effects , Hippocampus/metabolism , Lipid Peroxidation/drug effects , Male , Maze Learning/drug effects , Pregnancy , Rats , Rats, Wistar , Spatial Learning/drug effects , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism
2.
J Med Ethics Hist Med ; 10: 12, 2017.
Article in English | MEDLINE | ID: mdl-29416832

ABSTRACT

Consanguineous marriage, which is common in many regions in the world, has absorbed much attention as a causative factor in raising the incidence of genetic diseases. The adverse effects may be attributed to the expression of the genes received from common ancestors and mortality and morbidity of the offspring. Iran has a high rate of consanguineous marriages. In recent years genetic counseling has come to be considered in health care services. This cross-sectional study was conducted in order to determine the prevalence and types of consanguineous marriages in the genetic clinics in Isfahan. We aimed to define the different types of marriages, specific categories of genetic disorders associated with consanguineous marriages, and mode of inheritance in the family tree. We also narratively reviewed the ethical aspects of the issue. The data were collected using a simple questionnaire. A total number of 1535 couples from urban and rural areas formed the study population. The marriages were classified according to the degree of the relationship between couples, including: double cousin, first cousin, first cousin once removed, second cousin and beyond second cousin. The SPSS software version 16 was used for data analysis. Data obtained through genetic counseling offered during a 5-year period revealed that 74.3% had consanguineous relationships, 62.3% were first cousins, 1% were double cousins and 7.8% were second cousins. In addition, 76% of the couples had at least one genetic disease in their family tree. Related ethical issues were also considered in this study, including autonomy and informed decision making, benefit and harm assessment, confidentiality, ethics in research, justice in access to counseling services, financial problems ethics, and the intellectual property of scientific success.

3.
Food Chem Toxicol ; 96: 263-72, 2016 Oct.
Article in English | MEDLINE | ID: mdl-27421826

ABSTRACT

Either developmental lead or ethanol exposure can impair learning and memory via induction of oxidative stress, which results in neuronal damage. we examined the effect of combined exposure with lead and ethanol on spatial learning and memory in offspring and oxidative stress in hippocampus. Rats were exposed to lead (0.2% in drinking water) or ethanol (4 g/kg) either individually or in combination in 5th day gestation through weaning. On postnatal days (PD) 30, rats were trained with six trials per day for 6 consecutive days in the water maze. On day 37, a probe test was done. Also, oxidative stress markers in the hippocampus were also evaluated. Results demonstrated that lead + ethanol co-exposed rats exhibited higher escape latency during training trials and reduced time spent in target quadrant, higher escape location latency and average proximity in probe trial test. There was significant decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and increase of malondialdehyde (MDA) levels in hippocampus of animals co-exposed to lead and ethanol compared with their individual exposures. We suggest that maternal consumption of ethanol during lead exposure has pronounced detrimental effects on memory, which may be mediated by oxidative stress.


Subject(s)
Developmental Disabilities , Ethanol/toxicity , Hippocampus/drug effects , Lead/toxicity , Memory/drug effects , Oxidative Stress/drug effects , Spatial Learning/drug effects , Animals , Catalase/metabolism , Drug Combinations , Glutathione Peroxidase/metabolism , Lead Poisoning/etiology , Male , Malondialdehyde/metabolism , Maze Learning/drug effects , Rats , Rats, Wistar , Superoxide Dismutase/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL