The Killer tobacco plant, wild tobacco in the species of Nicotiana tabacum has been named by scientists recently in August 2021. It is found to have a unique feature of its kind.
Seven new species have been found and named but this buddy of ours is a different one. Just stay away from it or you may never know what it does(wink)
Alt: Killer Tobacco Plant.;
Image Description: They are found to be carnivorous.
Image Source :
Don’t think it’s some kind of a dangerous plant or something for us but yes, it has now posed a threat to the small insects around itself.
As mentioned earlier that it’s a new entrant to the insectivorous kingdom, we need to probe into this category of plant…
What’s so different?
The killer tobacco is found with several other species of the same family in the parched region of Australia by the scientists of Royal Botanica Gardens, Kew, Curtin University, and the University of Vienna.
Alt: The Royal Botanic Gardens at Kew, London.;
Image Description: The Kew Gardens where the killer tobacco got revealed.
They all belong to the same species of N. tabacum but the killer tobacco plant was named N. Insecticide.
The reason behind this nomenclature of the specific plant was:
● It contained sticky glands all over its surfaces which made the plant surface quite damp.
● This sticky surface helped the plant to abduct and kill some small insects like gnats, fleas, and aphids.
● No confirmation of any nutritional value being gained by the plant through the insects has been done.
● It is the first species of the tobacco plant to have been established as an ‘insect killer’.
These reasons have made the killer tobacco plant so peculiarly enthralling species of plant in the tobacco family.
Plant this in your house to get rid of insects…
An interesting story…
Can you guess the story as to how the scientists could crack this whole facade of the killer tobacco…??…
Let me take you through this intriguing tale…
Actually what happened is that its seeds were being collected by a truck stop on the Northwest Coastal Highway in Western Australia to be cultivated back in London in the greenhouses at Kew Gardens. When they were brought into London, they caught and killed the insects present in the nurseries.
Alt: Tobacco leaves.;
Image Description: Tobacco leaves are seen on a farm.
Image Source: https://www.pxfuel.com/en/free-photo-oazgf
Such a great twist in the tale of a plant(wink).
Though the studies are incomplete. Many other species are still left to be comprehended by our scientific researchers.
The research on this plant was successful during a collaborative study involving researchers in three countries namely the UK, Austria, and Australia. The research concerned the study of the existence of herbaceous species of plants in the harsh, arid region of dry Australia.
The results were worth the chase of eight long years….
Tobacco is derived from the leaves of the genus Nicotiana, a plant from the night-shade family, indigenous to North and South America.
Archeological studies suggest the use of tobacco in around first century BC, when Maya people of Central America used tobacco leaves for smoking, in sacred and religious ceremonies. It then later started spreading as far as high up to the Mississippi Valley with the Maya community migrating from down south of America, between 470 and 630 AD. Gradually, it was then adopted by neighboring and native tribes.
Native American “Shamans” developed tobacco use for religious rites. Simultaneously, people practicing medicine also started using tobacco in different forms to cure certain illnesses such as asthma, earaches, bowel problems, fever, sore eyes, depression, insect bites, burns, etc.
By the time Columbus and his successors documented tobacco in other countries, the natives started useing tobacco in pipes, cigars, and snuff. Subsequently, Portuguese and Spanish sailors helped to spread different forms of tobacco to be used, around the world.
Today, tobacco is used in various forms in different parts of the world. Tobacco in many countries is sometimes adopted as a cash crop by the farmers and government treasuries (excise, taxes, etc.), and is also grown for local consumption.
The major tobacco-growing and consuming countries are China, USA, the Former Soviet States, India, and Brazil. In South and Southeast Asia, it is incorporated into existing traditional customs, in the form of betel quid (paan) chewing.
The tobacco industry provides thousands of jobs, and is also a major source of income for the advertising industries, printed and electronic media, government (for revnew and as a source of foreign currency).
There are 2550 known compounds in tobacco and more than 4000 compounds in tobacco smoke.
Primary tobacco biohazardous compounds include at least 43 carcinogens, such as nicotine and nitrosamines, and alpha-emitting radionuclides such as polonium 210.
Tobacco smoke contains carbon monoxide, thiocyanate, herbicide, fungicide and pesticide residues, tars, and many other substances which promote diseases and impair the body’s defense mechanism and functions. Toxic substances in the tobacco smoke affect virtually every viable cell type.
First and foremost, adverse effect of smoking is immunosuppressive effect on the host, and hence adversely affecting host-parasite interactions.
The consumption of tobacco, whether inhaled, sniffed, sucked, or chewed, has evident harmful effects on health, and is addictive too. Scientists unequivocally evidenced that tobacco consumers suffer from three Ds: death, disease, and disability.
Different systems of our body are interrelated and they influence the use of any such product which is likely to cause health hazards affects many such body functions.
Its active ingredients, tar, nicotine, and nitrosamine, are potentially associated with oral cancer worldwide.
In the developed countries, smoking has been associated with over 85% deaths of all cancer deaths in men. It is estimated that 40–45% of all cancers and 90–95% of all lung cancers have an association with smoking. Many other diseases, such as chronic pulmonary obstructive disease (COPD) are implicated to cause death in 75% of the people between the age of 35 and 70 years. Many clinical study have established that pipe smoking has been associated with lip cancer.
While smokeless tobacco habits are endemic, oral cancer can account for more than one-third of all cancers. The prevalence of smoking in teenagers of India is increasing ranging from 19.7% to 34.5%.
ORAL AND SYSTEMIC EFFECTS OF SMOKING
Despite of increasing public awareness of risks associated with tobacco use and education programs to discourage its use, cigarettes and alcohol both are considered significant risk factors for a multitude of health consequences from the long-term and excessive use of either of these two.
It is ubiquitously accepted that smoking is a significant risk factor for cardiovascular diseases, COPD, and some forms of cancers. The use of any such product which is likely to cause health hazards, adversely affects functions of many systems.
Smokers have a characteristic change in color of exposed mucosal surfaces which is primarily due to melanin deposition on the basal cell layer of the mucosa. The relationship of a smoker’s melanosis (dark-brown foci) and inflammatory changes that result from heat, smoke, and inhalation with the absorption of exogenous pigments has not been determined. Tobacco-associated white keratosis patches are commonly found in smokers. Chronic smokers may also develop nicotine stomatitis (smoker’s palate). Verrucous carcinoma of Ackerman is a variant of squamous cell carcinoma and has an association with smokeless tobacco.
White keratosis of the buccal and tongue mucosa in a tobacco gutkha user
It has long been established that recurrent aphthous ulcer is a disease, almost exclusively, of nonsmokers. And this is one of the consistent findings. Recurrent aphthous ulcers may start if smoking is abandoned, although reasons are unclear.
Influence on periodontium
Arno et al. examined 1016 individuals for gingivitis and found a significant correlation between tobacco consumption and gingivitis when hygiene and age were kept constant. reviewed data from National Health and Nutrition Examination Survey and found that smokers had higher periodontal, debris, calculus, and oral hygiene index scores than non-smokers.
Smokers have greater susceptibility to periodontitis, and paradoxically less to gingivitis; the explanation given for this paradoxical clinical behavior is that probably smoking interferes with the inflammatory and immune response by activating endothelial and inflammatory cells to induce cytokines’ secretion. The deleterious effects of smoking on the periodontium include alteration in periodontal tissue vasculature, direct alternative effect on bacterial microflora, and the inhibitory effect on immunoglobulin levels and antibody responses to plaque bacteria. Nicotine is a vasoconstrictor, although its effects on gingivae have been proven to be difficult to measure.
It has been documented that tobacco components can have deleterious effects on various neutrophil functions (impaired chemotaxis/phagocytosis or both). Polymorphonuclear leukocytes motility, chemotaxis, and phagocytosis are significantly reduced in smokers. Thus this important first line of defense against subgingival bacteria is compromised in smokers. Antibody production is altered, specially opsonizing IgG2 and immune-regulatory T-cell subset ratio.
In this manner, both innate and acquired immune mechanisms are compromised in current smokers, allowing periodontal bacteria to escape host clearance and establish themselves as subgingival inhabitants.
Cigarette smoking increases bacterial adhesion to epithelial cells and has a differential effect on bacterial colonization, favoring growth of Gram-negative bacteria.
Alternation in the subgingival environment, such as decreased oxygen tension, allows, in turn, the overgrowth of an essentially anaerobic flora and overgrowth of opportunistic pathogenic microbial species. Periodontal pocket oxygen tension partial oxygen pressure (PO2) was significantly less in smokers compared with nonsmokers and was not influenced by gingival oxygen sufficiency.
Smokers are 2.6-6 times more likely to exhibit periodontal destruction than nonsmokers. Exposure to tobacco smoke is associated with an increased risk of adult periodontitis and increased disease severity in smokers compared to nonsmokers. It has been suggested in many studies that smokers have greater clinical attachment loss (CAL).
Attachment loss severity was increased by 0.5% by smoking 1 cigarette / day, while smoking up to 10-20 cigarettes increased the clinical attachment loss by 5-10%. A positive correlation has been established between serum levels of the nicotine metabolite cotinine and severity of CAL, probing depth, and alveolar crest height, because of which cigarette smoking significantly increases the risk for tooth loss by 70%.
Smokers appear to have a depressed number of helper lymphocytes (Th) which are important for B-cell function and antibody production. This has been manifested by decreased levels of salivary antibodies IgA and serum IgG. In smokers, a diminished serum IgG2 level and an impaired IgG2 response have been hypothesized to increase the risk of periodontitis.
Serum IgG antibodies to Prevotella intermedia and Fusobacterium nucleatum have also been reported to be reduced in smokers.
Pindborg noted that 98% of acute necrotizing ulcerative gingivitis (ANUG) patients studied were smokers. The effect of smoking appears to be complex than a mere reflection of patient stress. Clarke et al.. have demonstrated that the intra-arterial infusion of epinephrine and nicotine in rabbits resulted in reduced gingival blood flow rates in spite of increased systemic perfusion pressure.
Smokers who underwent periodontal surgery with either modified Widman flap or mucoperiosteal flap reflection had significantly less reduction in the pocket depth and gain in clinical attachment levels compared with nonsmokers. Root coverage following free gingival graft procedures is reportedly diminished by heavy cigarette smoking. Following regenerative procedures, the clinical attachment gain was les in smokers. Miller has reported a 100% correlation between failure to obtain root coverage and heavy smoking (more than 10 cigarettes/day). Heavy smokers who refrained from smoking during the first 2 weeks of healing had results comparable to nonsmokers.
Cigarette smokers have also been associated with a reduced healing response, after guided tissue regeneration (GTR) therapy in deep infrabony defects. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing.
An 80% failure rate in treatment of furcation defects using regenerative therapy has been seen in smokers. Nicotine may inhibit fibroblast-fibronectin and collagen production and increase the fibroblast collagenase activity.
Nicotine can also suppress the proliferation of cultured osteoblasts while stimulating the osteoblast alkaline phosphatase activity.
Tobacco components may also modify the production of cytokines or inflammatory mediators which play a role in periodontal tissue destruction.
Nicotine has been shown to increase the release of interleukin-6 by cultured murine osteoblasts. Smokers also have an increased crevicular fluid tumor necrosis factor-alpha (TNF- α) level.
Implant success rates are reduced in smokers. Smokers are 2.6 times more likely to have an implant failure between the time of implant uncovering and the time of restorative loading. A greater failure rate of implant in smokers has been seen in maxillary anterior teeth. Smoking may influence post-implant surgery healing and the long-term health of the peri-implant tissue. Many clinicians have reported smoking as an absolute risk factor in the selection of implant patients.
The risk of subgingival infection with Bacteroides forsythus in current smokers was 2.3 times that of former smokers or nonsmokers. The proportion of subjects positive for Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteroid forsythss were higher among smokers. Observational studies also report a greater level of plaque, calculus, and oral debris in smokers. This conclusion dominated for nearly two decades of clinical practice.
Cigarette smoking was also associated with increased levels of TNF- α in the crevicular fluid compared with non-smokers. The neutrophil elastase activity and levels of prostaglandin E2 (PGE2) and Matrix meatalloproteinase-8 (MMP8) were raised in smokers.
Nicotine, in addition, up-regulates LPS-mediated monocyte secretion of PGE2 and IL-1B. Free oxygen radicals from neutrophils are increased in smokers. Levels of metallothionine, a free-radical scavenger, are increased in the gingival tissue of smokers. Therefore, smoking appears to favor a pathogenic subgingival flora.
Nicotine has divergent effects on IL-1 and PGE2 secretion, depending upon the cell type and whether or not the bacterial components are present. Such alterations in the host response may affect the reparative and regenerative potential of the periodontium in tobacco users.
From the contemporary studies, a general pattern has emerged:
- Smokers have greater clinical attachment and alveolar bone loss.
- Increased number of deep pockets and calculus formation.
- Variable levels of plaque and inflammation.
A previous history of smoking does not appear to be deleterious to the response to periodontal therapy. It has been observed that occasionally, aphthae start when smoking is given up
Although bias is toward decreased signs of clinical inflammation
CONCLUSION AND COMMENTS
The association of tobacco and its products with several reversible and irreversible oral and systemic diseases and its manifestations have been ubiquitously established.
The adaptation of tobacco by either sex certainly has a familial or cultural impact.
Much has been done to produce, publicize, and popularize tobacco. In contrast negligible efforts are seen to discourage the practice of tobacco use, by the government, and NGOs.
In many countries,the health departments, trusts, and NGOs run voluntary services for smoking cessation at centers with various hospital services. Counseling to give up smoking is done by demonstrating the potential health hazards due to tobacco. Alcohol and tobacco are frequently used together and scientific research supports the popular observation that at large “smokers drink and drinkers smoke.”
Smoking has been identified as one of the major predictive variables for response in periodontal therapy. Studies on non-surgical therapy have shown less probing depth reduction and less attachment gain in smokers as compared to non-smokers. Similar results with less gain in bone height were found in patients’ undergone surgery.
Smoking has been considered as a significant risk factor in implant patients.
Wound healing is delayed in smokers as compared to nonsmokers.
Several studies suggest that smokers show a low response to maintenance therapy compared with non-smokers.
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-by SAMBHAVI YADAV