Expression of heat shock proteins 27, 60, and 70 in amphetamine and cocaine associated deaths. (December 2021)

• Record Type: Journal Article
• Authors: Madea, Burkhard; Ruppel, Elvira; Prangenberg, Julian; Krämer, Michael; Doberentz, Elke
• Is Part Of: Forensic science international. Volume 329(2021)
• Publication Date: 2021-12
• Subjects: Heat shock proteins -- Amphetamine- and cocaine-associated deaths -- Immunohistochemical expression; Medical jurisprudence -- Periodicals; Chemistry, Forensic -- Periodicals; Forensic Medicine -- Periodicals; Médecine légale -- Périodiques; Chimie légale -- Périodiques; Gerechtelijke geneeskunde; Gerechtelijke chemie; Gerechtelijke psychiatrie; Chemistry, Forensic; Medical jurisprudence; Electronic journals; Periodicals; Electronic journals; 614.1
• DOI: 10.1016/j.forsciint.2021.111088
• Languages: English
• ISSNs: 0379-0738

Abstract

Abstract: Introduction: The hearts of amphetamine and cocaine users demonstrate essentially the same microscopic features: hypertrophy, interstitial fibrosis, myocyte hypertrophy and intimal and medial hyperplasia. According to Karch (2016), some investigations suggest that amphetamines have properties that make users less likely to experience myocardial infarction than cocaine users. The exposure to amphetamine is associated with the production of heat shock proteins (HSP) whereas cocaine is not. Not all the HSP are present in normal living conditions of cells but their expression is increased when cells are exposed to stress, like heat, anoxemia, and ischemia. It has been known before that increased HSP production is a myocardial response in adaptation to cardiac ischemia and that the production of HSP might influence myocardial resistance to infarction. Furthermore, production of HSP is an explanation of the known ability of amphetamines to cause hyperthermia. The hypothesis of a cytoprotective function of HSP in amphetamine-associated deaths in comparison to cocaine-associated deaths and controls was investigated. Material and methods: Study group: 39 amphetamine-related fatal cases, 27 cocaine-associated deaths. Control group: 42 cases with other causes of death. Immunohistochemical staining of HSP 27, HSP 60, and HSP 70 in heart, liver, and kidney. Results: 16 out of 39 (41.0%) amphetamine-related fatal cases showed a positive HSP expression, predominantly HSP 70 in myocardial tissue. In cocaine-associated deaths 15 out of 27 (55.5%) cases were positive, also mainly HSP 70. In the kidney in amphetamine-associated deaths 18 out of 39 (46.1%) cases were positive, in cocaine-associated deaths 21 out of 27 (77.7%) cases. The cocaine group showed significantly increased expression for HSP 27 and 70 in the liver and HSP 70 in the kidney compared to the control as well as amphetamine group. Furthermore, the cocaine group showed significantly increased expression for HSP 27 and 70 in the heart compared to the control but not the amphetamine group. Conclusion: The hypothesis of Karch that in amphetamine-associated deaths a positive HSP expression has in contrast to cocaine-related deaths a cytoprotective function cannot be verified. Furthermore, cocaine and benzoylecgonine seem to independently lead to an increased expression of HSP 27 both in the liver and in the heart. Highlights: Heat shock proteins (HSP) are a group of proteins that belong to molecular chaperones. HSP are expressed in cells when there is exposure to variable stressful stimuli. Hyperthermia has been observed in amphetamine/methamphetamine (MA) abuse. It was speculated that HSP production in amphetamine abuse increases myocardial resistance to infarction. In this study both in cocaine and amphetamine fatalities a comparable HSP expression was found.