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2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) are persistent environmental contaminants that exist as complex mixtures in the environment, but the possible interactions of TCDD and PCBs have not been systematically investigated. The main objective of this study was to investigate the combined nephrotoxic effects of TCDD and PCBs on rats and to reveal the potential interactions between TCDD and PCBs. Male Sprague–Dawley rats were intragastrically administered TCDD (10 μg/kg), PCBs (Aroclor 1254, 10 mg/kg), or the combination (10 μg/kg TCDD + 10 mg/kg Aroclor 1254). After 12 consecutive days of exposure, all treatments induced nephrotoxicity, as evidenced by significant increases in the levels of serum creatinine and blood urea nitrogen, changes of kidney histopathology, and significant renal oxidative stress. Most of these effects were more remarkable in the combined-exposure group. Furthermore, all treatments induced renal cytochrome P450 1A1 (CYP1A1) protein expression, and the induction was more conspicuous in the combined-exposure group. These findings suggested that the nephrotoxicity induced by TCDD and PCBs in the present study might be attributable to the high expression of CYP1A1. In addition, the result of the two-way analysis of variance revealed that the combined effects of TCDD and PCBs were complicated, being additive, synergistic, or antagonistic depending on the selection of toxicity end points under the present experimental condition. This study demonstrates that combined exposure to TCDD and PCBs induced significant nephrotoxicity in rats, and there were complicated interactions between the two pollutants on the nephrotoxicity. [ABSTRACT FROM AUTHOR]

A fuzzy-controller design by the hybrid of genetic algorithm and particle-swarm optimisation (F-HGAPSO) is employed for a thyristor-controlled series capacitor (TCSC) to improve the transient stability of flexible AC transmission systems (FACTS). According to the variation of rotation speed, a fuzzy controller decides an approximate series capacitance to achieve a better dynamic response of FACTS. To design the fuzzy controller, a new design approach, the F-HGAPSO, is proposed. F-HGAPSO introduces the concept of the maturing phenomenon in nature into the evolution of individuals originally modelled by a genetic algorithm. The maturing phenomenon is mimicked by particle-swarm optimisation, where individuals enhance themselves based on social interactions and their private cognition. Simulations and comparisons with other approaches have demonstrated the effectiveness and efficiency of the proposed F-HGAPSO. [ABSTRACT FROM AUTHOR]

The present study was undertaken to observe the difference of nitrogen monoxidum (NO), malondialdehyde (MDA), cytochrome C (Cyt-C), nitric oxide synthase (NOS), mitochondrial calcium and superoxide dismutase (SOD) in myocardium between noninsulin dependent diabetes mellitus (NIDDM) rats and normal rats. Methods: Twenty NIDDM rats were made, and 20 normal rats were used as control. The levels of NO, MDA, Cyt-C, NOS, mitochondrial calcium and SOD in myocardial cells from all rats were measured, and histological changes were observed. Results: Compared with control, the levels of NO (2.28±0.40* vs 1.81±0.33 µmol/g protein), NOS (0.49±0.09* vs 0.39±0.07 U/mg protein), MDA (7.87±0.31* vs 7.36±0.53 nmol/mg protein), cytoplasma Cyt-C (3.68±0.17* vs 3.25±0.34 g/L) and mitochondrial calcium (2.90±0.35* vs 2.47±0.23 g/L) were higher (NIDDM rats vs control, *P<0.05) in the NIDDM rats. But, the levels of mitochondrial Cyt-C (0.19±0.05* vs 0.28±0.06 mmol/L) and mitochondrial SOD (0.81±0.21* vs 1.18±0.39 U/mg protein) were lower (NIDDM rats vs control, *P<0.05) in the NIDDM rats compared with control. Under microscope, myocardium deliquescenced and mitochondria swelled, and inflammatory cell infiltrated in mesenchyma. Conclusions: Oxyradical, lipid peroxidation, Cyt-C and mitochondrial calcium are involved in the damage of myocardium in NIDDM rats. [ABSTRACT FROM AUTHOR]

The present study was undertaken to observe the effects of ganoderan on mitochondrial Ca2+, cytochrome C, and cytosolic malondialdehyde (MDA), superoxide dismutase (SOD) in brain tissues from epilepsy rats. Methods: Epilepsy rats were made by intraperitoneal injection of sub-convulsive dosage of pentetrazole (PTZ, 32mg/kg/day for 21 days). Twenty epilepsy rats were divided into ganoderan-treated epilepsy group and vehicle-treated epilepsy group, and 10 normal rats were used as control. Flame atomic absorption spectrometry and spectrophotometric analysis were used to detect levels of mitochondrial Ca2+, SOD, MDA, and cytochrome C in brain tissues. Results: After treatment with ganoderan (by gastric gavage) for 28 days, the levels of mitochondrial Ca2+ (2.253±0.104 vs 2.132±0.115 mg/L) and cytochrome C (1.471±0.120 vs 1.168±0.095 mmol/L) were higher (ganoderan-treated epilepsy group vs vehicle-treated epilepsy group, P<0.05), and the levels of cytosolic cytochrome C (7.98±0.48 vs 8.67±0.61 mmol/L) and MDA (102.21±11.67 vs 105.29±18.99 mg/L) were lower (ganoderan-treated epilepsy group vs vehicle-treated epilepsy group, P<0.05), and the level of SOD (2301.04±155.24 vs 1863.27±186.68 U/mg protein) was higher (ganoderan-treated epilepsy group vs vehicle-treated epilepsy group, P<0.05) in the ganoderan-treated epilepsy rats than the vehicle-treated epilepsy rats. Conclusion: Ganoderan exerts protective effects on brain cell mitochondria in epilepsy by clearing free radical and strengthening antioxidation of brain tissues. [ABSTRACT FROM AUTHOR]

We have previously shown the antiepileptic effects of Ganoderma lucidum polysaccharides in in vitro studies; however, so far there is no such study reported in an in vivo model. In this study, the status epilepticus was induced in rats by kainic acid injection followed by G. lucidum polysaccharides treatment once a day for 7 days. Their epileptic behavior, electroencephalograph, along with the expression of caveolin-1, brain derived neurotrophic factor, nuclear factor kappa B, and hippocampal neuronal survival were assessed. Results showed that the epileptic behavior was improved significantly after G. lucidum polysaccharides treatments by a significant reduction of both the epileptic score and the duration of a heavy seizure attack while increasing both the epileptic latency and the time to heavy seizure attack. The epileptic electroencephalograph was ameliorated from previous sharp waves and frequent high amplitudes spikes to a group of scattering waves with lower frequency and small spikes. Furthermore, G. lucidum polysaccharides treatments enhanced the expression of caveolin-1, brain derived neurotrophic factor, and survivin, but decreased nuclear factor kappa B expression. These changes indicate that G. lucidum polysaccharides can alleviate epileptic seizure and this neuroprotective effect may be via increasing the expression of caveolin-1, brain derived neurotrophic factor, and survivin and decreasing the expression of nuclear factor kappa B in the hippocampal neurons. [ABSTRACT FROM AUTHOR]