Marijuana extracts possess the effects like the endocrine disrupting chemicals

Watanabe, Kazuhito; Motoya, Erina; Matsuzawa, Naoki; Funahashi, Tatsuya; Kimura, Toshiyuki; Matsunaga, Tamihide; Arizono, Koji; Yamamoto, Ikuo

doi:10.1016/j.tox.2004.08.005

Cited by 46 publications

(42 citation statements)

References 29 publications

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“…⌬ 9 -THC, ⌬ 9 -THCA, CBD, and CBDA were isolated and purified from the cannabis leaves according to the methods described elsewhere (Aramaki et al, 1968). Purities of these cannabinoids were checked to be at least 95 to 98% by gas chromatography (GC) (Watanabe et al, 2005). The crude extract from CBDA strain was prepared by the methods described previously (Watanabe et al, 2005) except that the crude extract was not treated with heating to decompose the acid forms (i.e., decarboxylation).…”

Section: Methodsmentioning

confidence: 99%

“…Purities of these cannabinoids were checked to be at least 95 to 98% by gas chromatography (GC) (Watanabe et al, 2005). The crude extract from CBDA strain was prepared by the methods described previously (Watanabe et al, 2005) except that the crude extract was not treated with heating to decompose the acid forms (i.e., decarboxylation). In fresh plant material, most of CBD has been reported to exist as its acid form (Turner et al, 1980).…”

Section: Methodsmentioning

confidence: 99%

“…In fresh plant material, most of CBD has been reported to exist as its acid form (Turner et al, 1980). The relative contents of CBDA (77%) and CBD (23%) were determined by thin-layer chromatography analysis using Fast Blue BB salt as a coloring reagent (Watanabe et al, 2005). To obtain more information GC analysis was used.…”

Section: Methodsmentioning

confidence: 99%

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Cannabidiolic Acid as a Selective Cyclooxygenase-2 Inhibitory Component in Cannabis

Takeda

Misawa²,

Yamamoto³

et al. 2008

Drug Metab Dispos

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113

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ABSTRACT:In the present study it was revealed that cannabidiolic acid (CBDA) selectively inhibited cyclooxygenase (COX)-2 activity with an IC 50 value (50% inhibition concentration) around 2 M, having 9-fold higher selectivity than COX-1 inhibition. In contrast, ⌬ 9 -tetrahydrocannabinolic acid (⌬ 9 -THCA) was a much less potent inhibitor of COX-2 (IC 50 > 100 M). Nonsteroidal anti-inflammatory drugs containing a carboxyl group in their chemical structures such as salicylic acid are known to inhibit nonselectively both COX-1 and COX-2. CBDA and ⌬ 9 -THCA have a salicylic acid moiety in their structures. Thus, the structural requirements for the CBDAmediated COX-2 inhibition were next studied. There is a structural difference between CBDA and ⌬ 9 -THCA; phenolic hydroxyl groups of CBDA are freed from the ring formation with the terpene moiety, although ⌬ 9 -THCA has dibenzopyran ring structure. It was assumed that the whole structure of CBDA is important for COX-2 selective inhibition because ␤-resorcylic acid itself did not inhibit COX-2 activity. Methylation of the carboxylic acid moiety of CBDA led to disappearance of COX-2 selectivity. Thus, it was suggested that the carboxylic acid moiety in CBDA is a key determinant for the inhibition. Furthermore, the crude extract of cannabis containing mainly CBDA was shown to have a selective inhibitory effect on COX-2. Taken together, these lines of evidence in this study suggest that naturally occurring CBDA in cannabis is a selective inhibitor for COX-2.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Cannabidiolic Acid as a Selective Cyclooxygenase-2 Inhibitory Component in Cannabis

Takeda

Misawa²,

Yamamoto³

et al. 2008

Drug Metab Dispos

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113

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“…CBD has also been reported to inhibit progesterone 17α-hydroxylase, testosterone 6α-hydroxylase, and testosterone 16β-hydroxylase [75]. However, CBD exhibits only weak efficacy as 10 mM CBD is required to inhibit~20%, 49%, and 67% of progesterone 17α-hydroxylase, testosterone 6α-hydroxylase, and testosterone 16β-hydroxylase, respectively.…”

Section: Enzymes Involve In Cholesterol Metabolismmentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

446

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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“…Regarding to the use of Cannabis, when studying mouse testis microsomes, it was reported that the extract of Cannabis sativa is capable of inhibiting the activity of CYP17A1 (P450c17), the enzyme responsible for the 17α-hydroxylation of progesterone and the subsequent formation of androstenedione, one of the substrates of aromatase (33). The authors also observed a similar result with the main constituents of Cannabis sativa, such as tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).…”

Section: Use Of Aromatase Inhibitorsmentioning

confidence: 99%

The use of aromatase inhibitors in boys with short stature: what to know before prescribing?

Linardi¹,

Damiani

Longui

2017

Arch. Endocrinol. Metab.

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Aromatase is a cytochrome P450 enzyme (CYP19A1 isoform) able to catalyze the conversion of androgens to estrogens. The aromatase gene mutations highlighted the action of estrogen as one of the main regulators of bone maturation and closure of bone plate. The use of aromatase inhibitors (AI) in boys with short stature has showed its capability to improve the predicted final height. Anastrozole (ANZ) and letrozole (LTZ) are nonsteroidal inhibitors able to bind reversibly to the heme group of cytochrome P450. In this review, we describe the pharmacokinetic profile of both drugs, discussing possible drug interactions between ANZ and LTZ with other drugs. AIs are triazolic compounds that can induce or suppress cytochrome P450 enzymes, interfering with metabolism of other compounds. Hydroxilation, N-dealkylation and glucoronidation are involved in the metabolism of AIs. Drug interactions can occur with azole antifungals, such as ketoconazole, by inhibiting CYP3A4 and by reducing the clearance of AIs. Antiepileptic drugs (lamotrigine, phenobarbital, and phenytoin) also inhibit aromatase. Concomitant use of phenobarbital or valproate has a synergistic effect on aromatase inhibition. Therefore, it is important to understand the pharmacokinetics of AIs, recognizing and avoiding possible drug interactions and offering a safer prescription profile of this class of aromatase inhibitors. Arch Endocrinol Metab. 2017;61(3):391-7.

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Marijuana extracts possess the effects like the endocrine disrupting chemicals

Cited by 46 publications

References 29 publications

Cannabidiolic Acid as a Selective Cyclooxygenase-2 Inhibitory Component in Cannabis

Cannabidiolic Acid as a Selective Cyclooxygenase-2 Inhibitory Component in Cannabis

Molecular Targets of Cannabidiol in Neurological Disorders

The use of aromatase inhibitors in boys with short stature: what to know before prescribing?

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