Role of oxidative stress and heme oxygenase activity in morphine-induced glomerular epithelial cell growth

Patel, Jaimita; Manjappa, Nagarathna; Bhat, Rajani; Mehrotra, P.; Bhaskaran, Madhu; Singhal, Pravin C.

doi:10.1152/ajprenal.00134.2003

Cited by 44 publications

(33 citation statements)

References 46 publications

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“…Morphine has a bimodal effect on GEC (190). At lower concentrations, morphine promotes GEC growth, whereas at higher concentrations, morphine triggers GEC apoptosis.…”

Section: Direct Effects Of Heroin/morphine On the Kidney: Pathophysiomentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased, the incidence of "heroin nephropathy" has declined. Because reports of heroin nephropathy predated the surveillance of hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities may be more associated with the development of nephropathy in heroin users than the drug's pharmacologic properties. Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.

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“…Morphine has a bimodal effect on GEC (190). At lower concentrations, morphine promotes GEC growth, whereas at higher concentrations, morphine triggers GEC apoptosis.…”

Section: Direct Effects Of Heroin/morphine On the Kidney: Pathophysiomentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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“…Higher concentrations of morphine triggered glomerular epithelial cell apoptosis. Free-radical scavengers as well as antioxidants inhibit morphine-induced pro-apoptotic effects, suggesting that the effects of morphine are mediated through oxidative stress [57]. A recent study showed that morphine increases intestinal ulcer formation and degradation of the host defense barrier.…”

Section: Physical Barriers: Epitheliamentioning

confidence: 99%

Opiate abuse, innate immunity, and bacterial infectious diseases

Wang

Barke

et al. 2008

Arch. Immunol. Ther. Exp.

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The first line of defense against invading bacteria is provided by the innate immune system. Morphine and other opiates can immediately disrupt the body's first line of defense against harmful external bacteria. Opiate, for example morphine, abuse degrades physical and physiologic barriers, and modulates phagocytic cells (macrophages, neutrophils) and, nonspecific cytotoxic T cells (gammadelta T), natural killer cells, and dendritic cells, that are functionally important for carrying out a rapid immune reaction to invading pathogens. In vitro studies with innate immune cells from experimental animals and humans and in vivo studies with animal models have shown that opiate abuse impairs innate immunity and is responsible for increased susceptibility to bacterial infection. However, to better understand the complex interactions between opiates, innate immunity, and bacterial infection and develop novel approaches to treat and even prevent bacterial infection in the opiate-abuse population, there is an urgent need to fill the numerous gaps in our understanding of the cellular and molecular mechanisms by which opiate abuse increases susceptibility to bacterial infection.

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“…Other studies linking opiates to oxidative stress focus on the determination of reactive oxygen species (ROS) in white blood cells (1), superoxide (17)(18)(19) or markers of oxidative damage such as malondialdehyde (MDA) (13,20,21), thiobarbituric acid reactive substances (TBARS), tissue carbonyl content (1,13) and isoprostane (3). Nevertheless, there is, to our knowledge, limited work on the evaluation of oxidative balance, as a whole, in heroin addicted individuals.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress is also implicated, as an underlying mechanism, in heroin-induced hepatotoxicity (27), as well as in the pathogenesis of renal lesions, such as focal and segmental glomerulosclerosis, secondary to heroin abuse (17,19,28). Researchers have even concluded that antioxidants can prevent the formation of such lesions.…”

Section: Discussionmentioning

confidence: 99%