Reduction of the Deleterious Effects of Tobacco Smoking by the Induction of Phase 2 Enzymes by Nerf2

a technology of nerf2 and enzymes, applied in the field of tobacco treatment, can solve the problems of compensatory oxidative stress or even oxidative damage, dna damage, etc., and achieve the effect of inhibiting or reducing the deleterious effects in a human body

Inactive Publication Date: 2008-01-24
SAVIPU PHARMA
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Benefits of technology

[0011] It has been discovered that smoking tobacco or a tobacco containing product containing or treated with an activator of Nerf2 acts to inhibit or reduce the deleterious effects in a human or other mammal caused by the smoking of tobacco when compared to untreated tobacco.
[0012] One aspect of the invention includes tobacco or a tobacco containing product containing or having applied thereto an effective amount of an activator of Nerf2 sufficient to prevent or reduce the deleterious effects on a mammal smoking the tobacco or tobacco product.
[0013] Another aspect of the invention includes a method for reducing the deleterious effects induced by tobacco smoking comprising incorporating an effective amount of a composition containing a Nerf2 into tobacco or a tobacco containing product prior to smoking the tobacco or tobacco product.

Problems solved by technology

An imbalance between the mechanisms that generate and protect against ROS results in compensatory oxidative stress or even oxidative damage, including DNA damage.

Method used

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  • Reduction of the Deleterious Effects of Tobacco Smoking by the Induction of Phase 2 Enzymes by Nerf2
  • Reduction of the Deleterious Effects of Tobacco Smoking by the Induction of Phase 2 Enzymes by Nerf2
  • Reduction of the Deleterious Effects of Tobacco Smoking by the Induction of Phase 2 Enzymes by Nerf2

Examples

Experimental program
Comparison scheme
Effect test

example 1

[0027] The rat tracheal epithelial (RTE) cell focus inhibition assay was used to identify potential chemopreventive activity of tanshinone IIA. Tanshinone IIA was evaluated for its ability to inhibit benzo[a]pyrene-induced transformation of RTE cells. Tracheal epithelial cells were isolated from 8-12 week-old male Fisher 344 rats and plated on collagen coated dishes. Initially, a nontoxic concentration of tanshinone IIA was determined by treating RTE cells with a range of 1.5 nM to 3000 nM of tanshinone IIA. Tanshinone IIA at concentrations of 150 nM and below was found to be nontoxic to RTE cells. About 10% cells survived at a concentration of 1500 nM. Freshly isolated RTE cells were exposed to benzo[a]pyrene alone or in combination with tanshinone IIA. Benzo[a]pyrene was washed out after an exposure of 24 h. The maximal non-toxic concentration and four half log concentrations of tanshinone IIA (300 nM to 3 nM) were used for the chemopreventive assay. After 30 days in culture, tran...

example 2

[0028] The same experiment is repeated except the administered dosage of the inhibitor of oxidative stress is delivered via the inhibitor applied to a tobacco sample which is in tern burned in the presence of cells. The results of the experiment are similar to example one and indicate this method of administration is effective to deliver an effective amount of inhibitor of oxidative stress to a mammal.

[0029] The tobacco was removed from a cigarette and weighed. Then, SP2010 and / or SP001P in chloroform (1 mg, 0.4 mg, and 0.02 mg) were added to the tobacco. The volume of chloroform was kept under 200 μL to ensure complete adherence to the tobacco. The material was dried, and the tobacco was repacked into the cigarette. The cigarette was loaded into a standard smoking machine and smoked. After smoking, both the filter and condensate were collected and dried. The condensate and filter samples were analyzed by HPLC (Shimadzu AHT2010) using water / methanol gradient, with a C18 reverse pha...

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Abstract

The invention features a method for inhibiting or reducing the deleterious effects of tobacco smoking including increased incidence of cancers, cardiovascular diseases, various lung disorders and the oxidative effects. The method includes the incorporation of an effective amount of a compound or a standardized plant extract that is that comprises an inhibitor of antioxidant stress due to the induction of phase 2 enzymes regulated by Nerf2 into tobacco or a tobacco product.

Description

[0001] This application claims priority of U.S. Application Ser. No. 60 / 807,685 filed on Jul. 18, 2006 and incorporated herein in its entirety by reference.Background of the Invention [0002] 1. Field of the Invention [0003] The field of the invention relates to the treatment of tobacco to lessen the deleterious effect of tobacco smoking. In particular the invention relates to the treatment of tobacco or a tobacco product with an effective amount of an inhibitor of oxidative stress due to the induction of phase 2 enzymes regulated by Nerf2 such that the deleterious effects of smoking tobacco are reduced. [0004] 2. Description of the Related Art [0005] Tobacco smoke (TS) is a major risk factor for a number of diseases including cancer, chronic obstructive pulmonary disease (COPD) and cardiovascular disease. Smokers have a high incidence of lung cancer, which is the most common cause of cancer in Western countries, accounting for more deaths than those caused by prostrate, breast, and ...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): A24B15/18
CPCA24D3/14A24B15/301
Inventor DEV, INDERJIT KUMARSUBBIAH, VEN
Owner SAVIPU PHARMA
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