• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.165-171
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• 2018

An overdose of antihypertensive agents, such calcium channel blockers (CCBs) and angiotensin II receptor blocker (ARBs), and the antihyperglycemic agent, metformin, leads to hypotension and lactic acidosis, respectively. A 40-year-old hypertensive and diabetic man with hyperlipidemia and a weight of 110 kg presented to the emergency room with vomiting, dizziness, and hypotension following an attempted drug overdose suicide with combined CCBs, ARBs, 3-hydroxy-3-methylglutaryl-coemzyme A reductase inhibitors, and metformins. A conventional medical treatment initially administered proved ineffective. The treatment was then changed to simultaneous extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT), which was effective. This shows that simultaneous ECMO and CRRT can be an effective treatment protocol in cases of ineffective conventional medical therapy for hypotension and lactic acidosis due to an overdose of antihypertensive agents and metformin, respectively.

• Journal of Dairy Science and Biotechnology
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• v.40 no.1
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• pp.15-22
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• 2022

This study evaluated the levels of D(-)-lactate and L(+)-lactate, and the ratio of D(-)-lactate to total lactate (D(-)-lactate + L(+)-lactate) of 15 lactic acid bacteria (LAB) using an enzymatic method. D(-)-lactate and L(+)-lactate levels in the LAB ranged from 0.31 to 13.9 mM and 0.76 to 39.3 mM, respectively, in Bifidobacterium sp.; 1.08 to 11.7 mM and 0.69-13.0 mM in Lactobacillus sp.; 0.72 to 20.3 mM and 0.98 to 32.3 mM in Leuconostoc sp., and 33.0 mM and 39.2 mM in Pediococcus acidilacti KCCM 11747. The ratio of the range of D(-)-lactic acid to total lactic acid was 28.98%-45.76% in Bifidobacterium sp., 41.18%-61.02% in Lactobacillus sp., 29.85%-42.36% in Leuconostoc sp., and 45.71% in P. acidilacti KCCM 11747. In the future, there is a need to test for D(-)-lactate in various fermented products to which different LAB have been added and study the screening of LAB used as probiotics that produce various concentrations of D(-)-lactate.

• Journal of Genetic Medicine
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• v.1 no.1
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• pp.39-43
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• 1997

The mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is inherited maternally, in which the MTTL1*MELAS 3243 mutation has been most commonly found as a heteroplasmy of A to G point mutation in the $tRNA^{Leu(UUR)}$ gene. The MTTL1*MELAS 3271 mutation is known to be the second common mutation, though clinical features of both mutations are not remarkably different. Recently, a variety of minor mutations have been reported in patients with MELAS. In this study, major efforts have been made to investigate the allele frequency of major three mutations including MTTL1*MELAS 3243, 3252, 3271 in 10 Korean families with MELAS probands. The PCR and subsequent direct sequencing of the PCR product in the regions spanning these three mutation sites were employed to identify the mutation in each proband. All family members have been screened for the presence of these three mutations by PCR-RFLP assay using Apa I, Acc I and Bfr I restriction enzymes. The MTTL1*MELAS 3243 mutation was most commonly found (7 out of 10 families tested) followed by the MTTL1*MELAS 3271 which was identified in 1 out of 10 families. In the remaining 2 families none of three mutations were found, indicating the presence of either nuclear mutation or yet unidentified mitochondrial DNA mutation in these families.

• Herbal Formula Science
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• v.18 no.2
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• pp.267-277
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• 2010

Objective : Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke like episodes (MELAS) syndrome is a progressive neurodegenerative disorder. The typical presentation of patients with MELAS syndrome includes features such as mitochondrial encephalomyopathy, lactic acidosis, and stroke like episodes. Other features, such as seizures, diabetes mellitus, hearing loss, cardiac disease, short stature, endocrinopathies, exercise intolerance, and neuropsychiatric dysfunction are clearly part of the disorder. Approximately 80% of patients with the clinical characteristics of MELAS syndrome have a genetic mutation. This progressive disorder is reported to have a high morbidity and mortality. This case report is intended to estimate clinical effects of oriental meedicinal treatment of MELAS syndrome. Methods : A 44 year old female patient diagnosed as MELSA syndrome was treated with general oriental medicinal therapy including acupuncture, moxibustion, cupping, pharmacupunture and herbal medication in 20XX in Wonkwang Medical Center Gwangju. And the changes in symptoms and signs were evaluated as time dependently. Results : Although there is currently no curable treatment and MEALS syndrome is tend to progress, our treatment showed improvement in general weakness, gait disturbance and pain in the patient. Conclusion : Our case report suggests that various oriental medicinal treatment could be effective for improvement of MELAS syndrome and may represent a new potential therapeutic approach to control the disease. It could be applied to improve general condition, prevent relapse, enhance the quality of life and reduce complaints in the patient.

• International Journal of Oral Biology
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• v.30 no.3
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• pp.85-90
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• 2005

Homeostatic pH is very important for various cellular processes, including metabolism, survival, and death. An imbalanced-pH might induce cellular acidosis, which is involved in many abnormal events such as apoptosis and malignancy. One of several factors contributing to the onset of metabolic acidosis is the production of lactate and protons by lactate dehydrogenase (LDH) in anaerobic glycolysis. LDH is an important enzyme that catalyzes the reversible conversion of pyruvate to lactate. This study sought to examine whether decreases in extracellular pH induce apoptosis of CHO cells, and to elucidate the role of mitogen-activated protein kinases (MAPKs) in acidification-induced apoptosis. To test apoptotic signaling by acidification we used CHO dhfr cells that were sensitive to acidification, and CHO/anti-LDH cells that are resistant to acidification-induced apoptosis and have reduced LDH activity by stable LDH antisense mRNA expression. In the present study, cellular lactic acid-induced acidification and the role of MAPKs signaling in acidification-induced apoptosis were investigated. Acidification, which is caused by $HCO{_3}^-$-free conditions, induced apoptosis and MAPKs (ERK, JNK, and p38) activation. However, MAPKs were slightly activated in acidic conditions in the CHO/anti-LDH cells, indicating that lactic acid-induced acidification induces activation of MAPKs. Treatment with a p38 inhibitor, PD169316, increased acidification-induced apoptosis but apoptosis was not affected by inhibitors for ERK (U0126) or JNK (SP600125). Thus, these data support the hypothesis that activation of the p38 MAPK during acidification-induced apoptosis contributes to cell survival.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.18 no.3
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• pp.95-98
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• 2018

A striking feature of mitochondrial disorders is the vast heterogeneity in their clinical symptoms that ranges from a single organ to severe multisystem involvement. Though a variety of ocular symptoms such as ptosis, pigmentary retinal degeneration, external ophthalmoplegia, and optic nerve atrophy can occur in association with mitochondrial cytopathies, progressive bilateral cataracts are rare among their ocular findings. A 5-year-old girl with no previous medical history came to our hospital presenting symptoms of seizure. She started showing progressive developmental regression, increased seizure frequency, hypotonia, general weakness, dysphagia and decreased vision. Lactic acidosis was noted in metabolic screening test and we confirmed mitochondrial respiratory chain complex I defect in spectrophotometric enzyme assay using the muscle tissue. Progressive bilateral cataracts then developed and were fully evident at the age of 7. She underwent cataract extraction with posterior chamber lens implantation. We are reporting a case of mitochondrial respiratory chain defect with multiorgan involvements including bilateral progressive cataract, an uncommon ocular manifestation. Ophthalmologic evaluation is highly recommended not to overlook the possible ocular manifestations in mitochondrial disorders.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.517-523
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• 2021

The present study aims to investigate the impact of hydrogen-rich water on the lactic acid level in metformin-treated diabetic rats under hypoxia. Thirty Sprague-Dawley rats were randomly divided into five groups, including normal diet group, and diabetes model (DM) group, DM + metformin treatment (DMM) group, DMM + hypoxia treatment (DMMH) group and DMMH + hydrogen-rich water (DMMHR) group. We found that the levels of lactic acid, pyruvate and lactate dehydrogenase were significantly lower in the blood of DMMHR group than DMMH group. Superoxide dismutase and glutathione levels in liver and heart were significantly higher in DMMH group after hydrogen-rich water treatment, while malondialdehyde and oxidized glutathione levels were decreased in DMMHR group when compared with DMMH group, which indicates that hydrogen-rich water could reduce oxidative stress. qPCR analysis demonstrated that that pro-apoptotic genes Bax/Caspase-3 were upregulated in DM group and metformin treatment suppressed their upregulation (DMM group). However, hypoxic condition reversed the effect of metformin on apoptotic gene expression, and hydrogen-rich water showed little effect on these genes under hypoxia. HE staining showed that hydrogen-rich water prevented myocardial fiber damages under hypoxia. In summary, we conclude that hydrogen-rich water could prevent lactate accumulation and reduce oxidant stress in diabetic rat model to prevent hypoxia-induced damages. It could be served as a potential agent for diabetes patients with metformin treatment to prevent lactic acidosis and reduce myocardial damages under hypoxic conditions.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.2
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• pp.102-108
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• 2016

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome is one of mitochondrial encephalopathy. As the early clinical manifestations can be variable, it is important to suspect the disease, especially in patients with multiple organ dysfunctions. A boy was diagnosed with epilepsy when he was 9 years old. Two years later, severe headache and blurred vision developed suddenly. On examination, left homonymous hemianopsia was detected with corresponding cerebral parenchymal lesions in right temporo-occipito-parietal areas. MELAS syndrome was confirmed by genetic test, which showed m.3243 A>G mitochondrial DNA mutation. Multivitamins including coenzyme Q10 were added to anticonvulsant. He experienced 4 more events of stroke-like episodes over 5 years, but he is able to perform normal daily activities. A 13-year-old boy was brought to the hospital due to suddenly developed respiratory arrest and asystole associated with pneumonia. Past medical history revealed that he had multiple medical problems such as epilepsy, failure-to-thrive, optic atrophy, and deafness. He has been on valproic acid as an anticonvulsant which was prescribed from local clinic. He recovered after the resuscitation, but his cognition and motor function were severely damaged. He became bed-ridden. He was diagnosed with MELAS syndrome by brain MRI, muscle biopsy, and clinical features. Genetic test did not reveal any mitochondrial gene mutation. Four years later, he expired due to suddenly developed severe metabolic acidosis combined with hyperglycemic hyperosmolar nonketotic coma. The clinical features of MELAS syndrome are variable. Early diagnosis before the presentation to the grave clinical course may be important for the better clinical outcome.

• 대한생식의학회:학술대회논문집
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• 2003.12a
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• pp.82-83
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• 2003

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.84-89
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• 2022

Vestibular dysfunction has rarely been reported in MELAS syndrome. A 40-year-old male with long-term diabetes and hearing loss experienced a stroke-like episode with hemisensory disturbance and lactic acidosis. Brain MRI showed temporo-parieto-occipital cortical lesions, and a final diagnosis was made of MELAS syndrome with the mitochondrial 3243A>G mutation. Neuro-otologic evaluations revealed anterior-canal-sparing bilateral impairments of the vestibulo-ocular reflex in the video head impulse test and no caloric paresis. This unique pattern of vestibular dysfunction may aid in diagnosing MELAS syndrome.