ABSTRACT
This research aimed to investigate the effect ofZingiber offi cinale Roscoe on Methyl parathionintoxication in rats. Methyl parathion (MP) is an organophosphate insecticide. Inhibition ofacetylcholinesterase is regarded as a direct toxic, whereas, its indirect role also induces oxidativestress, generates free radicals and alters the lipid membrane, resulting in cell damage or cell death.Ginger (Zingiber offi cinale Roscoe) is a traditional herbal medicine in Thailand, and it potentiallyreduces oxidative stress with antioxidant activity. In this study, rats were divided into 4 groups:control (normal diet), ginger diet, MP and MP with ginger diet. The study demonstrated that feedingthe rats with normal and ginger diet did not affect the AChE levels of red blood cells, which declinedwhen receiving are MP and MP with ginger diet. This result correlated with the AChE activity inmuscles, which was found to decrease in the number of motor endplates giving positive AChEactivity, and those motor endplates showed features of distortion and edema. The status of oxidativestress, as indicated by a lipid peroxidation marker (TBARS), showed that the highest TBARS wasobserved in the MP group. The ABTS radical cation decolorization assay found that ginger possessedantioxidant activity. In conclusion, oxidative stress was caused by low dose MP exposure and can beprevented by a ginger diet supplement.Chiang Mai Medical Journal 2010;49(3):81-88.
ABSTRACT
Background and objective: Although the electromagnetic radiation (EMR) emitted by mobile phones does not possess high energy like those of much higher frequencies such as X-rays and gamma-rays, several studies were reported with results showing that mobile phone use could produce hazardous health effects. These include headaches, changes in sleep patterns, electroencephalogram (EEG) and blood pressure. The present study was aimed to examine the effect of mobile phone exposure on brain oxidative stress. Methods: A group of about 300 g body weight male Wistar rats (EMR-exposed group) was put into re-straining cages and, after an equilibration period of at least 30 minutes, was exposed to a 900 MHz electromagnetic signal from two mobile phones (GSM system) at less than 10 cm distance for one hour in a day. This exposure was repeated for one week. Another group of animals (control group) served as a control and were subject to the same procedure but at more than 10 cm distance from the mobile phones. After the last exposure, the brains were removed, weighed and homogenized for determination of malondialdehyde (MDA) and glutathione (GSH). Results: The MDA concentrations in brain homogenates of the animals in the EMR-exposed group were not different from the control group of animals. Also, the GSH concentrations in the EMR-exposed group were at about the same levels as those in the control group. Conclusion: The present study provided no additional data indicating the probable role of oxidative stress in producing health effects of EMR exposure from mobile phone use.
ABSTRACT
Background: Dicrotophos is an organophosphate pesticide whose residue has been detected in most vegetables even in organic samples. Though this pesticide is classified as a highly hazardous Ib organophosphate, it is not banned in many countries including Thailand. Improper use of this chemical exposes the people to it through consumption of contaminated food and water. Some people develop signs of cholinergic syndrome following exposure and some suffer for days from paralysis of respiratory and limb muscles. However, there is no direct evidence indicating muscle weakness through decreased contractile property. All studies in humans thus far were clinically investigated and reported using information from subjective verbal histories. Objective: To investigate the contractile characteristics of skeletal muscles after dicrotophos exposure. Methods: A preliminary study was performed to determine the effective dose of dicrotophos that causes at least 30 % reduction in red blood cell cholinesterase activity. The rats were injected with dicrotophos daily at LD6.25, LD12.5 and LD25 doses for 5 weeks. It was found that the LD12.5 dose caused the effect, starting at the 4th week of injection. Therefore, this dose was injected into the rats before examining the isometric twitch characteristics of gastrocnemius muscle and cholinesterase activity in red blood cells and muscle homogenates. Results: Significant decreases in peak tension and time to peak tension were observed in rats exposed to this dose of dicrotophos. These decreases agreed with cholinesterase activity in RBC and muscle homogenates. Conclusion: Dicrotophos exposure in rats caused decreased contractile activity providing direct evidence implying the muscle weakness often found in humans.