Earticle

본 연구는 메스암페타민 의존자가 약물 사용 맥락에서 경험한 성적 착취 피해의 과정과 의미를 탐색하였다. 회복 과정을 거친 성인 6명을 대상으로 1:1 심층면담을 실시해 자료를 수집 하였다. 자료는 주제분석(Braun & Clarke, 2006)으로 분석하였다. 분석 결과 10개 주제(‘거 래성 성관계’, ‘강압적인 성행위’, ‘반복적 피해 경험’, ‘성욕 과다 및 충동 증가’, ‘일반적이지 않은 성행위’, ‘약물 권유를 통한 통제’, ‘상호 착취와 권력관계 순환’, ‘성욕 및 성적 회복 저 하’, ‘수치심 및 죄책감’, ‘파트너 관계 악화’)와 4개 차원(성 착취 피해/약물-성 상호작용/관 계 내 통제·권력/성기능·인식 변화 및 장애)이 도출되었다. 참여자들은 약물 확보·관계 유지 과정에서 성이 거래되거나, 판단력 저하 상태에서 강압적 성경험을 겪었다. 또한 성충 동 증가와 위험행동 확대, 통제와 권력 불균형, 피해-가해의 순환 구조가 확인되었다. 이 경 험은 단약 이후에도 수치심·죄책감, 관계 악화, 성기능 저하로 이어져 통합적 개입의 필요 성을 시사한다.

This study explored the processes and meanings of sexual exploitation experienced by individuals with methamphetamine dependence within the context of drug use. Data were collected through in-depth, one-on-one interviews with six adults who had entered recovery. The data were analyzed using thematic analysis (Braun & Clarke, 2006). The findings yielded ten themes (“transactional sexual relationships,” “coercive sexual experiences,” “recurrent victimization,” “heightened sexual desire and impulsivity,” “non-normative sexual behaviors,” “control through drug inducement,” “cyclical power dynamics of mutual exploitation,” “decline in sexual desire and recovery,” “shame and guilt,” and “deterioration of partner relationships”) and four overarching dimensions (sexual exploitation victimization; drug sexuality interaction; relational control and power; and changes and impairments in sexual functioning and perception). Participants reported that sexual activities were often commodified in the process of obtaining drugs or maintaining relationships, and that coercive sexual experiences occurred under impaired judgment due to substance use. Increased sexual impulsivity, expansion of risky behaviors, power imbalances, and cyclical shifts between victimization and perpetration were also identified. These experiences persisted beyond abstinence, leading to shame, guilt, relational deterioration, and sexual dysfunction, thereby highlighting the need for integrated intervention approaches.

본 연구에서는 오랫동안 약물에 의존하는 삶을 살아왔지만, 지금은 단약 중인 전 폭력조직원의 생애를 회복관점으로 접근하면서, 이를 통해 필로폰을 비롯한 다양한 약물에 의존하게 하거나 중지하게 만든 요인들을 교정복지 차원에서 탐 구하고자 하였다. 자료 수집과 분석은 Rosenthal의 내러티브-생애사 인터뷰 분석 (Narrative-Biographical Interview Analysis)방법을 사용하였다. 분석을 통해 전 폭력조직원이 약물에 의존하게 만들었던 요인들과 약물에서 벗어나게 만든 요인 들을 사회문화적 내지는 법·제도적인 측면에서 검토하였다. 연구 결과, 약물에 의 존하는 삶을 살았던 전 폭력조직원에게 영향을 미쳤던 요인들은 다양하게 나타 났다. 또한, 참여자의 이야기된 생애사를 재구성하는 과정에서 참여자는 약물을 하면서 살았던 자신의 지난 삶을 ‘허송세월’로, 단약 이후 참여자가 살아가고 있 는 삶은 ‘자전거 페달 밟기’와 ‘끊어진 끈 잇기’로 의미화되고 있음을 알 수 있었 다. 결론 및 논의에서는 법적, 사회적 측면에서 치료와 재활을 위한 생태적 환경 구축의 필요성을 제시하였다.

In this study, we have lived a drug-dependent life for a long time, but we have approached the recovery point of the life of a former gang member who is now on a short-lived basis, to explore the factors that have led him to rely on or stop a variety of drugs, including methamphetamine. To this end, Rosenthal's Narrative-Biological Interview Analysis method, which suggests that data collected be analySed through five stages, was used, and the analysis was reviewed in terms of legal and cultural aspects that led all gang members from adolescence to adulthood to factors that led to drug dependence and factors that led to their release from drugs. Studies have shown a variety of factors that have affected former gang members who have lived drug-dependent lives. In addition, in the process of reconstructing a participant's talked-about life history, participants were able to see that their past life as a drug was meant to be 'spend his life in vain' and that life in which participants lived after a short period of time was meant to be 'bicycle pedaling' and 'broken stringing.' The conclusions and discussions presented the need for the establishment of an ecological environment for treatment and rehabilitation in legal and social aspects.

마약류의 남용이 국가에 미치는 영향은 마약류남용자의 숫자나 정도 및 이와 연계된 범죄조직의 규모 등에 따라 다를 수 있다. 그러나 공통적으로는 건강사회의 장애, 가정의 파괴, 실업, 인력의 손실, 이들의 예방이나 치료를 위한 사회보장 비용의 지출 등 경제 전반에 직접‧간접적인 영향을 미치게 되어 국력약화와 전 국민의 정신적‧신체적 황폐화를 초래한다. 또한 마약류 남용으로 인한 환각상태에서의 강력범죄의 범행, 금단증상에 의한 동기 없는 범죄, 마약류 구입자금 마련을 위한 강력사범의 증가 등 심각한 사회병리현상으로 전이된다. 현재 한국의 마약류관련범죄는 숫자상으로는 안전지대로 볼 수 있으나, 체감으로 느끼는 범죄의 심각성은 이미 안전정도를 넘어서고 있다. 특히 최근 마약류단속인원의 증가, 마약류 남용 계층의 확산, 마약류 압수량의 급증, 마약류 공급선의 다변화‧다양화 추세, 조직폭력배의 마약류 범죄개입, 외국인 마약사범의 증가 현상은 한국이 더 이상 마약의 안전지대가 될 수 없음을 보여 준다. 따라서 무엇보다도 마약류범죄에 대한 체계적인 대책수립이 필요하다. 한국이 그동안 어렵게 지켜온 마약안전지대로서의 위상을 유지하고, 마약류 남용국가로 전락되는 것을 미연에 방지하기 위하여서는 마약수사 역량강화를 위한 예산과 인력의 대폭 확충 및 재범방지를 위한 마약류 중독자 치료․재활센터 보강 등 범정부적 차원의 우선적 지원이 필요한 시점이다. 더불어 마약류범죄에 대한 범국민적 관심과 참여가 필요하다. 국민 모두가 마약류범죄에 대한 감시자가 되어 신고와 협조체제가 이루어진다면 마약류범죄에 대한 가장 효과적인 대책이 될 것이다. 또한 마약류범죄에 대한 국제적 정보교환 및 사법공조 등 협력체제가 활성화되어야 할 것이며 한국의 수사당국은 이를 위해 적극적․능동적으로 이에 대처해 나가야 한다.

The effect of methamphetamine on the pulmonary metastasis was investigated in C57BL/6 mice injected with Bl6 melanoma cells. Bl6 melanoma cells (2$\times$10$^{5}$ cells) were injected intravenously into 5~7 weeks old C57BL/6 mice. Mice were then treated intraperitoneally with methamphetamine either acutely (two times with one week interval) or subchronically (daily for 14 days). Degree of pulmonary metastasis was investigated and specific immunologic parameters such as natural killer cell cytotoxicity(NKCC), antibody-dependent cellular cytotoxicity(ADCC) and blastogenic responses of splenocytes were examined. Mice which had been subchronically treated with methamphetamine showed significant decreases in the number of pulmonary metastasis of Bl6 melanoma cells, NKCC and ADCC without a significant change in blastogenic responses. In the acutely-treated group, slight trends of decrease in the numbers of pulmonary metastasis, NKCC and ADCC were observed without statistical significances whereas there was a significant increase in blastogenic responses. The mechanism underlying the decrease in the degree of metastasis despite diminished NKCC and ADCC after methamphetamine treatment and the relationship between the degree of pulmonary metastasis and duration of methamphetamine treatment remain to be investigated.

BALB/C mice were intraperitoneally injected with methamphetamine (5 mg/kg) to observe the effect of methamphetamine on the immune system. Body weights were decreased in both acutely treated group (twice for 2 weeks with 7 days interval) and subchronically treated group (daily injection for 14 days). The relative spleen weights and the numbers of splenocytes were unexpectedly increased (p<0.05) in acutely treated group, but subchronically treated group showed the trend of decrease without significance. But there was no significant effect on antibody formation to hen egg Iysozyme which was immunized during the treatment of methamphetamine and on plaque forming cell number. The relative thymus weights of both groups were significantly decreased by the treatment of methamphetamine (acutely treated group, p<0.05; subchronically treated group, p<0.01). These results suggest that the effect of methamphetamine on the immune system may be caused by thymic dysfunction.

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.

Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) have become popular recreational drugs of abuse in many countries. Although the neurotoxic damage caused by METH and MDMA is characterized by degeneration of the dopaminergic and serotonergic systems in brain, the molecular and cellular mechanisms remain to be clarified. Therefore, the purposes of this study were to confirm the capability of METH and MDMA to induce apoptosis and to clarify the action of its molecular mechanism by using serotonergic JAR cells and dopaminergic SK-N-SH cells. METH and MDMA were dose-dependently cytotoxic to human serotonergic JAR cells and dopaminergic SK-N-SH cells. The morphological change of apoptosis was found in Giemsa staining and TUNEL and further verified in DNA fragmentation analysis. Immunoblotting analysis revealed proteolytic cleavage of caspase-3 and -9 and change of bcl-2 and bax proteins. These results suggest that METH and MDMA may induce caspase-dependent apoptosis via the mitochondrial cell death pathway and METH and MDMA-induced neurotoxicity may happen to broadly and independently of both dopaminergic and serotonergic systems.

Methamphetamine (MA) is one of the most commonly abused drugs in the world by illegal drug users. Addiction to MA is a serious public health problem and effective therapies do not exist to date. It has also been reported that behavior induced by psychostimulants such as MA is related to histone deacetylase (HDAC). MeBib is an HDAC6 inhibitor derived from a benzimidazole scaffold. Many benzimidazole-containing compounds exhibit a wide range of pharmacological activity. In this study, we investigated whether HDAC6 inhibitor MeBib modulates the behavioral response in MA self-administered rats. Our results demonstrated that the number of active lever presses in MA self-administered rats was reduced by pretreatment with MeBib. In the hippocampus of rats, we also found MA administration promotes GluN2B, an NMDA receptor subunit, expression, which results in sequential activation of ERK/CREB/BDNF pathway, however, MeBib abrogated it. Collectively, we suggest that MeBib prevents the MA seeking response induced by MA administration and therefore, represents a potent candidate as an MA addiction inhibitor.

Limonene is a cyclic terpene found in citrus essential oils and inhibits methamphetamine- induced locomotor activity. Drug dependence is a severe neuropsychiatric condition that depends in part on changes in neurotransmission and neuroadaptation, induced by exposure to recreational drugs such as morphine and methamphetamine. In this study, we investigated the effects of limonene on the psychological dependence induced by drug abuse. The development of sensitization, dopamine receptor supersensitivity, and conditioned place preferences in rats was measured following administration of limonene (10 or 20 mg/kg) and methamphetamine (1 mg/kg) for 4 days. Limonene inhibits methamphetamine- induced sensitization to locomotor activity. Expression of dopamine receptor supersensitivity induced by apomorphine, a dopamine receptor agonist, was significantly reduced in limonenepretreated rats. However, there was no significant difference in methamphetamine-induced conditioned place preferences between the limonene and control groups. These results suggest that limonene may ameliorate drug addiction-related behaviors by regulating postsynaptic dopamine receptor supersensitivity.

Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.

Methamphetamine (METH) is a powerful neurotoxic psychostimulant affecting dopamine transporter (DAT) activity and leading to continuous excess extracellular dopamine levels. Despite recent advances in the knowledge on neurobiological mechanisms underlying METH abuse, there are few effective pharmacotherapies to prevent METH abuse leading to brain damage and neuropsychiatric deficits. α-Pinene (APN) is one of the major monoterpenes derived from pine essential oils and has diverse biological properties including anti-nociceptive, anti-anxiolytic, antioxidant, and anti-inflammatory actions. In the present study, we investigated the therapeutic potential of APN in a METH abuse mice model. METH (1 mg/kg/day, i.p.) was injected into C57BL/6 mice for four alternative days, and a conditioned place preference (CPP) test was performed. The METH-administered group exhibited increased sensitivity to place preference and significantly decreased levels of dopamine-related markers such as dopamine 2 receptor (D2R) and tyrosine hydroxylase in the striatum of the mice. Moreover, METH caused apoptotic cell death by induction of inflammation and oxidative stress. Conversely, APN treatment (3 and 10 mg/kg, i.p.) significantly reduced METH-mediated place preference and restored the levels of D2R and tyrosine hydroxylase in the striatum. APN increased the anti-apoptotic Bcl-2 to pro-apoptotic Bax ratio and decreased the expression of inflammatory protein Iba-1. METH-induced lipid peroxidation was effectively mitigated by APN by up-regulation of antioxidant enzymes such as manganese-superoxide dismutase and glutamylcysteine synthase via activation of nuclear factor-erythroid 2-related factor 2. These results suggest that APN may have protective potential and be considered as a promising therapeutic agent for METH-induced drug addiction and neuronal damage.

Repeated administration of psychostimulants such as amphetamines increases locomotor activity in rodents. These drugs, including methamphetamine, enhance dopaminergic neurotransmission and result in hyper-locomotion and behavioral sensitization. It is well known that the existence of a complex balance between the cholinergic and dopaminergic systems in the central nervous system. Thus, behavioral sensitization by methamphetamine may be related to the expression of the M1 muscarinic acetylcholine receptors gene. The present study investigated the changes of M1R mRNA in hyperlocomotor activity and behavioral sensitization by methamphetamine (2 mg/kg) in mice. Our results showed that M1R mRNA expression was increased in the frontal cortex and the hippocampus region (the CA2 region) in the acute methamphetamine administered group compared to the saline administered group. In the chronic group, M1R mRNA expression was increased in the frontal cortex ill1d the hippocampus regions (CA2 and DG regions) in melt1amphetamine administered group compared to saline control group. These results indicate that acute or chronic treatment of mathamphetamine leads to the region-specific changes in mRNA expression levels of M1R. Therefore, Therefore, the present result suggests that M1R may play a role in modulating of methamphetamine-induced behavioral sensitization in mice.