Enhanced tumor growth in brain dopamine-depleted mice following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment

Basu, Sujit; Dasgupta, Partha; Chowdhury, Jayasree Roy

doi:10.1016/0165-5728(95)00044-3

Cited by 30 publications

(17 citation statements)

References 27 publications

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“…It is possible that dopamine, or DRD1 , has tumor suppressive functions (45, 46). However, as dopamine cannot cross the blood brain barrier logic suggests that the relationship is somehow mediated outside of the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

A DRD1 Polymorphism Predisposes to Lung Cancer among Those Exposed to Secondhand Smoke during Childhood

Robles

Yang

Jen

et al. 2014

Cancer Prevention Research

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Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6 and DRD1 were mined for single nucleotide polymorphisms (SNPs) that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3’UTR SNP in DRD1 (Dopamine Receptor D1) was associated with a lower risk of lung cancer among individuals exposed to secondhand smoke during childhood (OR: 0.69; 0.60, 0.79; P<0.0001). This relationship was evident in both ever (OR: 0.74; 0.62, 0.88; P=0.001) and never smokers (OR 0.61; 0.47, 0.79; P<0.0001), European American (OR: 0.65; 0.53, 0.80; P<0.0001) and African American (OR: 0.73; 0.62, 0.88; P=0.001) populations. While much remains undefined about the long-term risks associated with exposure to secondhand smoke and heterogeneity between individuals in regard to their susceptibility to the effects of secondhand smoke, our data show an interaction between a SNP in the 3’UTR of DRD1 and exposure to secondhand smoke during childhood. Further work is needed to explore the mechanistic underpinnings of this SNP and the nature of the interaction between DRD1 and exposure to secondhand smoke during childhood.

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Section: Discussionmentioning

confidence: 99%

A DRD1 Polymorphism Predisposes to Lung Cancer among Those Exposed to Secondhand Smoke during Childhood

Robles

Yang

Jen

et al. 2014

Cancer Prevention Research

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“…However, several humoral factors released into the circulation during exercise can also modulate NKCA. NKCA is stimulated by increased concentrations of certain circulating cytokines (IL-2, IL-6, TNF-a and IFN-c; Benzcur et al 1984;Henney et al 1981;Jewitt et al 1996;Luger et al 1989), b-endorphin (Fiatarone et al 1989) and dopamine (Basu et al 1995;Deleplanque et al 1994), but is reduced in response to prostaglandin E 2 (Pedersen et al 1990). By expressing total cytolytic activity per NK cell, we have demonstrated that the single-cell cytolytic activity was unaltered by any of the three dierent types of exercise adopted here.…”

Section: Impact Of Three Dierent Types Of Exercise On Nk Cellsmentioning

confidence: 96%

Impact of three different types of exercise on components of the inflammatory response

Brenner¹,

et al. 1999

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It was hypothesized that muscle injury would be greater with eccentric than with all-out or prolonged exercise, and that immune changes might provide an indication that supplements the information provided by traditional markers such as creatine kinase (CK) or delayed-onset muscle soreness. Eight healthy males [mean (SE): age = 24.9 (2.3) years, maximum oxygen consumption (VO2(max)) = 43.0 (3.1) ml x kg(-1) x min(-1)] were each assigned to four experimental conditions, one at a time, using a randomized-block design: 5 min of cycle ergometer exercise at 90% VO2(max) (AO), a standard circuit-training routine (CT), 2 h cycle ergometer exercise at 60% VO2(max) (Long), or remained seated for 5 h. Blood samples were analyzed for CK, natural killer (NK) cell counts (CD3(-)/CD16(+)56(+)), cytolytic activity and plasma levels of the cytokines interleukin (IL)-6, IL-10, and tissue necrosis factor alpha (TNF-alpha). CK levels were only elevated significantly 72 h following CT. NK cell counts increased significantly during all three types of exercise, but returned to pre-exercise baseline values within 3 h of recovery. Cytolytic activity per NK cell was not significantly modified by any type of exercise. Prolonged exercise induced significant increases in plasma IL-6 and TNF-alpha. We conclude that the lack of correlation between traditional markers of muscle injury (plasma CK concentrations and muscle soreness rankings) and immune markers of the inflammatory response suggests that, for the types and intensities of exercise examined in this study, the exercise-induced inflammatory response is modified by humoral and cardiovascular correlates of exercise.

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“…In support of this hypothesis, a dopaminergic system injury has also been shown to cause an enhanced tumor growth [8]. Moreover, 6-hydroxydopamine (6-OHDA) treatment, which reduces both dopamine and norepinephrine concentrations in the CNS, impairs humoral immune responsiveness and activation of spleen T suppressor lymphocytes [9].…”

Section: Introductionmentioning

confidence: 95%

MPTP-induced central dopamine depletion exacerbates experimental autoimmune encephalomyelitis (EAE) in C57BL mice

Bałkowiec-Iskra

Kurkowska‐Jastrzębska

Joniec

et al. 2007

Inflamm. res.

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It is obvious that the central nervous system plays a role in the regulation of an immune response. However, the mechanisms of this regulation are poorly understood. The goal of the present study was to examine the role of one of the neurotransmitters - dopamine, in this process. We used experimental autoimmune encephalomyelitis (EAE), an autoimmune disease with its effector phase in the CNS, as a model to study the effect of central dopamine depletion on the development of an immune response. Dopamine depletion was achieved by treatment with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropiridine (MPTP; 40 mg/kg), whereas EAE was elicited by immunization with MOG 35-55 (150 microg) in complete Freund's adjuvant (CFA), supplemented with Mycobacterium tuberculosis. As determined by HPLC, striatal dopamine contents in mice treated with MPTP were significantly lower compared to vehicle-treated controls. Remarkably, striatal depletion of dopamine prior to EAE induction resulted in an earlier onset of the disease and an augmentation of its clinical signs. Moreover, the striatal dopamine-depleted mice demonstrated an increased concentration of IL-1beta and decreased concentration of TGFbeta in the spinal cord, compared to EAE mice. Since MPTP itself does not have any direct effect on immune cells, it strongly suggests that the observed changes in EAE induction and progression after MPTP administration depended on lower dopamine level. Further studies are required to find out the cellular mechanism of the dopamine action.

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Enhanced tumor growth in brain dopamine-depleted mice following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment

Cited by 30 publications

References 27 publications

A DRD1 Polymorphism Predisposes to Lung Cancer among Those Exposed to Secondhand Smoke during Childhood

A DRD1 Polymorphism Predisposes to Lung Cancer among Those Exposed to Secondhand Smoke during Childhood

Impact of three different types of exercise on components of the inflammatory response

MPTP-induced central dopamine depletion exacerbates experimental autoimmune encephalomyelitis (EAE) in C57BL mice

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