• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.10b
• /
• pp.117-117
• /
• 2003

Bee Venom (BV) has been treated in inflammatory diseases such as rheumatoid arthritis (RA). Bee venom contains several biologically active non-peptide substances as well as two major known peptides; the hemolytic peptide melittin (50%) and the neurotoxic peptide apamin, and a number of minor peptides.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.10b
• /
• pp.130-130
• /
• 2003

Methylmercury (MeHg) is a well-known neurotoxicant that causes severe damage to the central nervous system in humans. Many reports have shown that MeHg is poisonous to human body through contaminated foods and has released into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established so far.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.10b
• /
• pp.139-140
• /
• 2003

Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of Alzheimer's disease (AD), and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD. In the present study, we investigated the effect of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on inflammatory cell death induced by beta-amyloid, a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.10b
• /
• pp.64-67
• /
• 2003

Halogenated aromatic hydrocarbons (HAHs) including TCDD and PCBs are known to cause neurotoxic effects in both man and animals such as cognitive impairment and motor dysfunctions. While theses chemicals may lead to neurodevelopmental and neurobehavioral deficit, structural activity relationship and molecular targets for these chemicals are not elucidated.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2002.11b
• /
• pp.191-191
• /
• 2002

Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of Alzheimer's disease (AD), and nonsteroidal anti-inflammatory drugs have been shown to retard the progress of AD. In this study, we have investigated the molecular mechanisms underlying oxidative and inflammatory cell death induced by beta-amyloid (Abeta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD, in cultured PC12 cells.(omitted)

• Biomolecules & Therapeutics
• /
• v.28 no.5
• /
• pp.381-388
• /
• 2020

Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.

• Clinical and Experimental Pediatrics
• /
• v.62 no.2
• /
• pp.43-47
• /
• 2019

Hyperammonemia can be caused by several genetic inborn errors of metabolism including urea cycle defects, organic acidemias, fatty acid oxidation defects, and certain disorders of amino acid metabolism. High levels of ammonia are extremely neurotoxic, leading to astrocyte swelling, brain edema, coma, severe disability, and even death. Thus, emergency treatment for hyperammonemia must be initiated before a precise diagnosis is established. In neonates with hyperammonemia caused by an inborn error of metabolism, a few studies have suggested that peritoneal dialysis, intermittent hemodialysis, and continuous renal replacement therapy (RRT) are effective modalities for decreasing the plasma level of ammonia. In this review, we discuss the current literature related to the use of RRT for treating neonates with hyperammonemia caused by an inborn error of metabolism, including optimal prescriptions, prognosis, and outcomes. We also review the literature on new technologies and instrumentation for RRT in neonates.

• Proceedings of the PSK Conference
• /
• 2003.04a
• /
• pp.271.2-271.2
• /
• 2003

The ${\gamma}$- and ${\beta}$-secretase are one of the most important proteases, which cleave amyloid precursor protein (APP) into neurotoxic A${\beta}$ peptide in Azheimer's type dementia. In the course of screening for anti-dementia agents from natural products, the mycelial culture of mushroom Phellinus linteus showed potent inhibition againt ${\beta}$-secretase (BACE1). (omitted)

• Proceedings of the PSK Conference
• /
• 2003.10b
• /
• pp.93.1-93.1
• /
• 2003

Bee Venom (BV) has been treated in inflammatory diseases such as rheumatoid arthritis (RA). Bee venom contains several biologically active non-peptide substances as well as two major known peptides; the hemolytic peptide melittin (50%) and the neurotoxic peptide apamin, and a number of minor peptides. Previous our study showed that BV blocked LPS and SNP-induced production of NO and PG through inactivation of NF-kB which regulates expression of COX-2 and iNOS. (omitted)

• Proceedings of the PSK Conference
• /
• 2003.10b
• /
• pp.116.1-116.1
• /
• 2003

Bisphenol A (BPA) mimics estrogen and its activity is one third to one quarter that of estradiol. BPA, an ubiquitous environmental contaminent has been shown to cause development reproductive toxicity and carcinogenic effect. BPA may do physiological action through ER$\alpha$ and ER$\beta$ which are expressed in central nerve system. We previously found that expose of BPA to immature mice resulted in behavial alternation, suggesting that overexposure of BPA could be neurotoxic. (omitted)