Turpentine Oil

The term 'turpentine oil' derives from the Latin word terebinthine, the name of the terebinth tree, and has been traditionally employed as an aseptic agent in the preparation of ointments and Zomad in the Iranian traditional medicine.

From: Encyclopedia of Toxicology (Third Edition) , 2014

Volatile oils and resins

William Charles Evans BPharm BSc PhD DSc FIBiol FLS FRPharmS , ... Daphne Evans BA MA , in Trease and Evans' Pharmacognosy (Sixteenth Edition), 2009

TURPENTINE OIL

Pharmaceutical turpentine oil is obtained by distillation and rectification from the oleoresin produced by various species of Pinus. The unrectified oil is the turpentine of commerce. The resin remaining in the still is the source of colophony (q.v. under 'Resins').

Rectification of the commercial oil consists of treatment with aqueous alkali to remove traces of phenols, cresols, resin acids etc. and possible redistillation.

The genus Pinus is widely distributed and many countries have considerable reserves of pine forest. The principal species employed are (1) Pinus palustris (longleaf pine) and P. elliottii (slash pine) in the S. and S.E. United States; (2) P. pinaster (P. maritima) in France, Italy, Portugal and Spain; (3) P. halepensis in Greece and Spain; (4) P. roxburghii (P. longifolia) in India and Pakistan; (5) P. massoniana and P. tabuliformis in China; (6) P. carribaea var. hondurensis and P. oocarpa in Central America and (7) P. radiata in New Zealand.

The collection of the oleoresin is very labour-intensive and for this reason output in the USA has declined considerably. Principal world producers are now Portugal and China; other contributors, in addition to the USA, include Spain, Greece, Morocco, France, India, the former USSR, Honduras and Poland. Many other countries produce smaller quantities for their own use. It is considered that about 250 000 trees are required to sustain a small commercial processing plant.

Oil of turpentine is a colourless liquid with a characteristic odour and a pungent taste. It is soluble in alcohol, ether, chloroform and glacial acetic acid. Oil of turpentine is optically active, but the rotation varies not only with the species of pine from which it has been obtained, but also

in samples taken from the same tree at different periods. Samples taken from the same tree at different times have given rotations varying from −7° 27′ to +18° 18′ in the case of Pinus palustris, and −28° 26′ to +1° 23′ in the case of Pinus heterophylla. The French oils from Pinus pinaster are strongly laevorotatory (−20° to −38°). Over forty components have been identified in French turpentine oil derived from P. pinaster.

Oil of turpentine consists chiefly of the terpenes (+)- and (−)-α-pinene, (−)-β-pinene and camphene. These tend to undergo atmospheric oxidation, with the formation of complex resinous substances, the removal of which is accomplished by the process of rectification mentioned above. The varying optical rotations of differing turpentines are mainly due to the varying proportions of the (+)- and (−)-α-pinenes present; (−)-β-pinene is found in almost all Pinus spp. in a high state of optical purity and typically occurs with the predominantly (+)-α-pinene. These two isomers have opposite absolute configurations. Other components of the oil which find industrial uses are β-phellandrene, δ-3-carene (a major component of Indian and 'Russian' turpentines), limonene, p-cymene, longifoline and estragol.

Oil of turpentine is now rarely given internally. Externally it is used as a counterirritant and rubefacient. For inhalation, terebene is usually preferred. Terebene is prepared from oil of turpentine by the action of cold sulphuric acid, which converts the pinene into the optically inactive (±)- limonene (dipentene). Now, most turpentine is processed to give its various constituents which find use in the manufacture of fragrances, flavours, vitamins, insecticides, etc.

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Turpentine

S. Saeidnia , in Encyclopedia of Toxicology (Third Edition), 2014

Background

The term 'turpentine oil' derives from the Latin word terebinthine, the name of the terebinth tree, and has been traditionally employed as an aseptic agent in the preparation of ointments and Zomad in the Iranian traditional medicine. In general, turpentine is a liquid gained via distillation of resin from live trees, particularly pines, while the Persian turpentine tree or the Mount Atlas mastic tree (Pistacia atlantica) is the main source of terebinth and mastic growing in the wild in southern Iran. The preparation of turpentine (the physiological or pathological exudates from conifers) possibly originated in the Caucasus and its southwestern spurs as well as in central and northern Europe during the Middle Ages. The dense pine forests of the south Atlantic states are the main sources of the North American industry, which was developed in the eighteenth century, especially in Virginia and the Carolinas. Although in the past turpentine had no or limited application in household economy, distillation of turpentine resulted in the oil that was introduced to medicine and materia medica during medieval times. Turpentine is a well-known essential oil extracted by distillation from pine oleoresin. The oleoresin itself is provided by tapping trees of the genus Pinus. The solid phase left behind after distillation is known as rosin. Both turpentine and rosin have various applications, but only turpentine is discussed in detail here. Gum naval stores (including gum turpentine and gum rosin) are distinguishable from turpentine and rosin, which have been recovered as by-products from chemical pulping of pines. Turpentine oil is composed of terpene hydrocarbons (including α-pinene, β-pinene, limonene, 3-carene, and camphene), together with other oxygenated terpenes such as anethole. However, its proportions may be different, depending on the source of the product.

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The nervous system

Robert Tisserand , Rodney Young PhD , in Essential Oil Safety (Second Edition), 2014

Turpentine oil

Craig (1953) reported 16 cases of turpentine oil ingestion, all in children of 5 years or under. There were convulsions in two of these cases, infants of 13 and 14 months, the older child having ingested 4  oz (~   102   mL), and the younger child an unknown quantity. A fatal case involving convulsions was reported in a child of 11 months, who had been given two teaspoons of spirits of turpentine by her grandmother, who said she thought the baby had worms. The child was distressed before the turpentine was given, she had a temperature of 103   °F, and findings on post-mortem included an enlarged thymus and acute bronchitis. It is therefore possible that the turpentine was not the principal cause of either the convulsions or the fatal outcome (Harbeson 1936).

The only cases involving seizures appear to be in infants who ingested very large quantities of turpentine essential oil, but none of its constituents are known to be convulsant. Consequently turpentine oil should not be regarded as presenting a general convulsant risk.

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Animal Models of Molecular Pathology

Carolyn Cray , in Progress in Molecular Biology and Translational Science, 2012

A Comparison to Other Markers of APR

An experimental model of inflammation using the injection of turpentine oil in dogs provides data which demonstrate the differences among the various inflammatory markers ( Fig. 2). 86 Levels of IL-6 and TNF-α were increased within a few hours with maximal response at 12–24   h postinjection. While an early increase (marginal response) in total white blood cells (WBC) was observed, the higher magnitude response was not present until days 4–7. A gradual decrease in serum albumin was present through day 14. The maximal decrease was less than 50% of day 0 values. CRP levels were increased 400-fold by day 2 postinjection and normalized by day 14. Serum AGP was increased approximately twofold on a similar timeline with maximal levels on day 3. Similar results can be found in a study of LPS injection in a model of arthritis in horses. 87 An early increase in WBC occurs within 24   h of the stimulus. SAA increases by 24   h with peak values at 48   h and elevated levels through day 5.

Fig. 2. Comparison of expression of acute inflammatory biomarkers after the injection of turpentine oil in a dog. Arrows indicate time of peak expression. Horizontal lines indicate period of expression.

APP are commonly compared to WBC and fibrinogen as they are long-standing hallmarks of inflammatory processes. In a large study of samples from dogs with various inflammatory processes, only a weak correlation (r  =   0.44) was observed between CRP levels and WBC counts but no correlation to the presence of band neutrophils which generally indicate bone marrow stimulation. 88 In a smaller study, a poor correlation (r  =   0.34) was observed between the CRP and the presence of band neutrophils. 89 A positive correlation was observed between HP and FIB in dogs with various diseases. 90 In a study of horses with various conditions, SAA and FIB were found to be consistently elevated in those animals with bacterial infection, whereas low or normal total WBC and neutrophil counts were observed. 91

In our own laboratory, we have compared inflammatory markers in both dogs and horses with various diseases (C. Cray, 2011). The mean total WBC values, while significantly higher than the control group, did not exceed normal reference intervals for this determination. Similarly, there was a mild decrease in the A/G ratio and a mild increase in the fibrinogen between the clinical groups. Changes for all these determinations were less than twofold. Notably, a 70- and 20-fold mean increase was observed for SAA and CRP in horses and dogs, respectively. It is this magnitude of difference which makes the clinical use of APP especially attractive. 5 As major APP are normally either not present or present in very low levels, increases are rapid and persistent as other minor and moderate APP are produced during later stages of inflammation.

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Development & Modification of Bioactivity

Yoshiaki Noma , Yoshinori Asakawa , in Comprehensive Natural Products II, 2010

3.19.2.2.6(ii) β-Pinene (337 and 337′)

(+)-β-Pinene ( 337 ) is found in many essential oils. Optically active and racemic β-pinene are present in turpentine oils, although in smaller quantities than (+)-α-pinene ( 130 ). 41

Shukla et al. 209 obtained a similarly complex mixture of transformation products from (−)-β-pinene ( 337′ ) through degradation by a Pseudomonas sp. (PL strain). On the other hand, Bhattacharyya and Ganapathy 210 indicated that A. niger NCIM 612 acts differently and more specifically on the pinenes by preferably oxidizing (−)-β-pinene ( 337′ ) at the allylic position to form the interesting products pinocarveol ( 349a′ ) and pinocarvone ( 352 ), besides myrtenol ( 333′ ) (see Scheme 152 ). Furthermore, the conversion of (−)-β-pinene ( 337′ ) by P. putida-arvilla (PL strain) gave borneol ( 332 ) ( Scheme 152 ). 68

Scheme 152. Structures of (+)- ( 337 ) and (−)-β-pinene ( 337′ ), and biotransformation of (−)-β-pinene ( 337′ ) by Aspergillus niger NCIM 612, Pseudomonas putida-arvilla (PL strain), and Pseudomonas pseudomallai.

Pseudomonas pseudomallai isolated from local sewage sludge by an enrichment culture technique utilized caryophyllene as the sole carbon source. 211 Fermentation of (−)-β-pinene ( 337′ ) by P. pseudomallai in a mineral salt medium (Seubert's medium) at 30   °C with agitation and aeration for 4 days yielded camphor ( 353′ ), isoborneol ( 332b′ ), borneol ( 332a′ ), α-terpineol ( 80′ ), and β-isopropyl pimelic acid ( 140′ ) ( Scheme 152 ). Using a modified Czapek–Dox medium and keeping the other conditions the same, the pattern of the metabolic products was dramatically changed. The metabolites were trans-pinocarveol ( 349a′ ), myrtenol ( 333′ ), α-fenchol ( 354a′ ), α-terpineol ( 80′ ), myrtenic acid ( 334′ ), and two unidentified products ( Scheme 152 ). 211

(−)-β-Pinene ( 337′ ) was converted by the plant pathogenic fungus B. cinerea to four new compounds, namely (−)-pinane-2α,3α-diol ( 355′ ), (−)-6β-hydroxypinene ( 356 ), (−)-4α,5-dihydroxypinene ( 357 ), and (−)-4α-hydroxypinen-6-one ( 358 ) ( Scheme 153 ). 212 (−)-Pinane-2α,3α-diol ( 355′ ) and related compounds were further biotransformed by microorganisms as shown in Scheme 153 .

Scheme 153. Biotransformation of (−)-β-pinene ( 337′ ) by Botrytis cinerea, (+)- ( 337 ) and (−)-β-pinene ( 337′ ) by Aspergillus niger TBUYN-2, and (−)-β-pinene ( 377′ ) and (+)-trans-pinocarveol ( 349a′ ) by Aspergillus niger TBUYN-2.

As shown in Scheme 153 , (+)- ( 337 ) and (−)-β-pinenes ( 337′ ) were biotransformed by A. niger TBUYN-2 to (+)-α-terpineol ( 80 ) and (+)-oleuropeyl alcohol ( 210 ) and their antipodes ( 80′ and 210′ ), respectively. The hydroxylation process of α-terpineol ( 80′ ) to oleuropeyl alcohol ( 210 ) was completely inhibited by 1-aminobenzotriazole, a cytochrome P-450 inhibitor. 204

(−)-β-Pinene ( 337′ ) was at first biotransformed by A. niger TBUYN-2 to (+)-trans-pinocarveol ( 349a′ ). 213 (+)-trans-Pinocarveol ( 349a′ ) was further transformed by three pathways: in the first pathway, (+)-trans-pinocarveol ( 349a′ ) was metabolized to (+)-pinocarvone ( 352a′ ), (−)-3-isopinanone ( 359 ), (+)-2α-hydroxy-3-pinanone ( 360b′ ), and (+)-2α,5-dihydroxy-3-pinanone ( 361b′ ); in the second pathway, (+)-trans-pinocarveol ( 349a′ ) was metabolized to (+)-6β-hydroxyfenchol ( 362a′ ); and in the third pathway, (+)-trans-pinocarveol ( 349a′ ) was metabolized to (−)-6β,7-dihydroxyfenchol ( 363a′ ) via epoxide and diol as intermediates ( Scheme 153 ). 213

(−)-β-Pinene ( 337′ ) was metabolized by A. niger TBUYN-2 via three pathways as shown in Scheme 154 to give (−)-α-pinene ( 130′ ), (−)-α-terpineol ( 80′ ), and (+)-trans-pinocarveol ( 349a′ ). (−)-α-Pinene ( 130′ ) was further metabolized by three pathways. At first, (−)-α-pinene ( 130′ ) was metabolized via (−)-α-pinene epoxide ( 131′ ), trans-sobrerol ( 125a′ ), (−)-8-hydroxycarvotanacetone ( 262 ), and (+)-8-hydroxycarvomenthone ( 276 ) to (+)-p-menthane-2,8-diol ( 100a′ ), which is also formed from (−)-carvone ( 104 ) metabolism. Second, (−)-α-pinene ( 130′ ) was metabolized to myrtenol ( 333′ ), which is metabolized by rearrangement reaction to give (−)-oleuropeyl alcohol ( 210′ ). (−)-α-Terpineol ( 80′ ), which is formed from β-pinene ( 337′ ), was also metabolized to (−)-oleuropeyl alcohol ( 210′ ), and (+)-trans-pinocarveol ( 349a′ ) formed from (−)-β-pinene ( 337′ ) was metabolized to pinocarvone ( 352′ ), 3-pinanone ( 359 ), 2α-hydroxy-3-pinanone ( 360b′ ), 2α,5-dihydroxy-3-pinanone ( 361b′ ), and 2α,9-dihydroxy-3-pinanone ( 366a′ ). Furthermore, (+)-trans-pinocarveol ( 349a′ ) was metabolized by rearrangement reaction to 6β-hydroxyfenchol ( 362a′ ) and 6β,7-dihydroxyfenchol ( 363a′ ) ( Scheme 154 ). 213

Scheme 154. Biotransformation of (−)-α-pinene ( 130′ ), (−)-β-pinene ( 337′ ), and related compounds by Aspergillus niger TBUYN-2.

(−)-β-Pinene ( 337′ ) was metabolized by A. niger TBUYN-2 to (+)-trans-pinocarveol ( 362a′ ), which was further metabolized to 6β-hydroxyfenchol ( 362a′ ) and 6β,7-dihydroxyfenchol ( 363a′ ) by a rearrangement reaction ( Scheme 155 ). 213 6β-Hydroxyfenchol ( 362a′ ) was also obtained from (−)-fenchol ( 354a′ ). (−)-Fenchone ( 368′ ) was hydroxylated by the same fungus to give 6β- ( 367b′ ) and 6α-hydroxy-(−)-fenchone ( 362b ). There is a close relationship between the metabolism of (−)-β-pinene ( 337′ ) and those of (−)-fenchol (354a′) and (−)-fenchone ( 368′ ).

Scheme 155. Relationship between the metabolism of (−)-β-pinene ( 337′ ), (+)-fenchol (354′), and (−)-fenchone (368′) by Aspergillus niger TBUYN-2.

(−)-β-Pinene ( 337′ ) and (−)-α-pinene ( 130′ ) were isomerized to each other. Both were metabolized via(−)-α-terpineol ( 80′ ) to (−)-oleuropeyl alcohol ( 210′ ) and (−)-oleuropeic acid ( 368′ ). (−)-Myrtenol ( 333′ ) formed from (−)-α-pinene ( 130′ ) was further metabolized via cation to (−)-oleuropeyl alcohol ( 210′ ) and (−)-oleuropeic acid ( 76 ). (−)-α-Pinene ( 130′ ) was further metabolized by A. niger TBUYN-2 via (−)-α-pinene epoxide ( 131′ ) to trans-sobrerol ( 125a′ ), (−)-8-hydroxycarvotanacetone ( 252′ ), (+)-8-hydroxycarvomenthone ( 276a′ ), and mosquitocidal (+)-p-menthane-2,8-diol ( 100a′ ) ( Scheme 156 ). 1,204,214,215

Scheme 156. Metabolic pathways of (−)-β-pinene ( 337′ ) and related compounds by Aspergillus niger TBUYN-2.

The major metabolites of (−)-β-pinene ( 337′ ) were trans-10-pinanol (myrtanol) ( 364 ) (39%) and (−)-1-p-menthene-7,8-diol (oleuropeyl alcohol) ( 210′ ) (30%). In addition, (+)-trans-pinocarveol ( 349a′ ) (11%) and (−)-α-terpineol ( 80′ ) (5%) were also formed. Verbenol ( 331a′ and 331b′ ) and pinocarveol ( 349a′ ) were oxidation products of α- ( 130′ ) and β-pinene ( 337′ ), respectively, in the bark beetle Dendroctonus frontalis. (−)-cis- ( 331a′ ) and (+)-trans-Verbenols ( 331b′ ) have pheromonal activity in Ips paraconfussus and Dendroctonus brevicomis, respectively ( Scheme 157 ). 207

Scheme 157. Metabolism of (−)-β-pinene ( 337′ ) by bark beetle, Dendroctonus frontalis.

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Composition of essential oils and other materials

Sue Clarke BSc (Hons) PhD , in Essential Chemistry for Aromatherapy (Second Edition), 2008

35 Juniper (Juniper communis)

AROMAFACT

The essential oil extracted from the berries by steam distillation is considered to be superior to that from the twigs and leaves. The wood oil is often adulterated with turpentine oil and it is advisable to avoid it for aromatherapy.

The water white essential oil has a slightly woody-balsamic and refreshing odour. Its main chemical components are the monoterpenes α-pinene (26–71%), β-pinene (1.5–13.9%), limonene (2.3–41%), sabinene (0.2–8.9%), β-myrcene (2.5–9.8%) and others in lower amounts, the aromatic hydrocarbon p-cymene (1.1–5.2%), alcohol terpinene-4-ol (2.1–9.7%) and oxide 1,8-cineole (0.5–4.0%). A certificate of analysis is shown in Box 7.24 with the accompanying spectra in Box 7.25. Historically juniper was used to treat contagious diseases and the British Herbal Pharmacopoeia cites its use for cystitis and rheumatism. Its partnership with gin is well known. It is regarded as an efficient detoxifier and diuretic with extracts used commercially in diuretic and laxative preparations. It is frequently applied to problems of the urino-genital system. However, it has been suggested that the essential oil may be a kidney irritant when levels of pinenes are high, as found in essential oil extracted from needles and branches. The essential oil from the berry is also employed for stress and anxiety relief and believed to ease menstrual pains. In skincare it is suited to oily and congested complexions and conditions such as eczema, psoriasis and dermatitis. It is considered to be nontoxic and nonsensitizing but there have been reports of irritant reactions. It should not be used on anyone with kidney disease or during pregnancy as it may stimulate the uterine muscles. Safety data is illustrated in Box 7.23.

Figure 7.18. Juniper berry. Analysis of Juniperus communis, showing a typical composition.

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Toxicity

Robert Tisserand , Rodney Young PhD , in Essential Oil Safety (Second Edition), 2014

Contact dermatitis

Most cases of contact dermatitis to essential oils are allergic as distinct from irritant, but in the context of this chapter, the difference is largely academic. Dermatologists have carried out thousands of patch tests using essential oils or, more commonly, constituents. This provides valuable information in terms of comparing the relative potencies of substances. However, only a small percentage of those reacting positively to a patch test actually have a skin problem that has been caused by an essential oil.

Only those essential oils used in patch testing can contribute to statistics, and the ones that are most commonly tested—sandalwood oil, jasmine absolute, narcissus absolute, tea tree oil, ylang-ylang oil—tend to be those used in previous patch tests. There are many reports of tea tree oil reactions (see below), but we could find none for narcissus absolute or sandalwood oil. There are a small number of cases each for ylang-ylang oil and jasmine absolute, as there are also for black seed oil and laurel leaf oil, though these last two are not routinely used in patch testing.

The essential oils used in patch testing also tend to be those for which allergenic constituents have not been identified. Testing does not usually include, for example, cinnamon bark oil, since its major constituent, cinnamaldehyde, is routinely used in patch testing. We found four cases of cinnamon oil allergy (presumably bark oil) over a 30 year period: one caused by skin contact with the undiluted oil (Sparks 1985), two from an ointment containing cinnamon oil (Calnan 1976), and one from a cinnamon oil mud bath (Garcéa-Abujeta et al 2005).

Skin allergies often follow an epidemiological pattern:

•

a new cosmetic ingredient is introduced

•

there are virtually no reports of adverse reactions

•

its use becomes widespread

•

over the course of several decades, reports of adverse reactions escalate

•

use of the ingredient is restricted or otherwise reduced

•

reports of adverse reactions decline.

Turpentine oil was a well-known contact allergen for a long time, mainly through occupational exposure, but when the mass paint industry replaced it with petroleum-based substitutes for paint thinning, reported cases of turpentine oil allergy decreased ( Schnuch et al 2004a). Similarly, cold-pressed laurel berry oil (which contains some essential oil) was widely used as a conditioner for felt hats for about 100 years (1860–1960). By the 1940s it was recognized as a major cause of dermatitis, and the felt industry ceased using laurel oil in 1962. Since 1975, there have been no reports of laurel berry oil allergy.

Not every widely used essential oil causes skin problems. We found four case reports of confirmed dermatitis from citronella oil, but all of them were from contact with the undiluted oil and none of them is recent (Keil 1947; Lane 1922). Considering the extensive application of citronella oil in insect repellants for many decades, the apparent lack of skin reactions is notable. Similarly, in spite of the widespread use of lavender oil in the West since about 1990, we could only find only five confirmed instances of dermatitis from 1991–2000: two involved the undiluted oil being dripped onto pillows at night and causing facial dermatitis (Coulson & Khan 1999), two were cases with multiple sensitivities to essential oils (Schaller & Korting 1995; Selvaag et al 1995), and one was an aromatherapist with hand dermatitis (Keane et al 2000).

Reported cases of tea tree oil allergy are more prevalent for this period. For the years 1991–2000, we found 29 cases, and in 21 of them the undiluted oil was used (Apted 1991; De Groot & Weyland 1993; Elliott 1993; Knight & Hausen 1994; Selvaag et al 1994, 1995; De Groot 1996; Bhushan & Beck 1997; Hackzell-Bradley et al 1997; D'Urben 1998; Rubel et al 1998; Khanna et al 2000; Varma et al 2000; Vilaplana & Romaguera 2000). One case was caused by airborne vapors, another by ingestion of the essential oil.

Even these few examples illustrate the increased risk of using undiluted essential oils on the skin. Single case reports are not a highly accurate reflection of incidence, since some cases are unrecorded. They do, however, give an approximation of the extent of a problem.

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Camphor

H.L. Rivera , F. Barrueto , in Encyclopedia of Toxicology (Third Edition), 2014

Environmental Fate and Behavior

Camphor is a white or transparent, waxy or crystalline substance with a strong aromatic odor. The boiling point is 204 °C and melting point is 176–180 °C. Camphor sublimates at room temperature and standard atmospheric pressure. Camphor has a specific gravity of 0.99, relative vapor density of 5.2, and vapor pressure of 20 Pa at 20 °C. Its solubility in water is 0.125 g per 100 ml water at 25 °C and it is soluble in ethanol, ethyl ether, turpentine, and essential oils.

Camphor vaporizes easily and is degraded in the atmosphere by reaction with photochemically produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 1.6 days. If released to soil, camphor is expected to have moderate mobility, based on an estimated K oc of 470. Volatilization from moist soil surfaces is expected to be an important fate process, based on an estimated Henry's Law constant of 8.1 × 10−5 atm-m3 mol− 1. Camphor may volatilize from dry soil surfaces based on its vapor pressure. If released into water, camphor may adsorb to suspended solids and sediment, based on the estimated K oc. Biodegradation is not expected to be an important environmental fate process in water or soil, based on its persistence in water. Estimated volatilization half-lives for a model river and model lake are 10 h and 9 days, respectively.

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Urolithiasis and Nephrocalcinosis in Childhood

Bernd Hoppe , ... Dawn S. Milliner , in Comprehensive Pediatric Nephrology, 2008

History of Urolithiasis

Kidney stone disease has been known since ancient times as documented by different archaeologic findings as well as writings about painful stone colic and attempts at stone treatment, including removal. In earlier centuries, urolithiasis was often a disastrous disease, all too often leading to the patient's death.

The examination of Egyptian mummies revealed kidney and bladder stone disease, such as a 5000-year-old bladder stone in the funeral site of El Amrah. Regimens for treatment were found in the papyrus Ebers (1500 BC), which is the main source of information about traditional Egyptian medicine. Saltpeter and turpentine oil were known to increase urine production, and pulverized eggshell (mainly from ostrich eggs) with a high content of calcium carbonate was ingested to intestinally bind lithogenic substances.

Sushruta, who was the main physician of Kaniska, the king of India (circa 6th century BC), was the first to describe stone removal via the urethra using a splint. Some time later, he recommended the so-called "Steinschnitt" procedure. Although many patients died during this procedure, it was still the only possible intervention. "Stein Schneider," who were people who removed urinary stones, were traveling throughout Europe until the late 18th century. Because most of the patients were boys between the ages of 9 and 14 years, it is assumed that stone disease was most prevalent among this age group.

The prevalence of kidney stone disease increased during the 16th, 17th, and 18th centuries among all ages and social groups. During the late 17th century Frére Jacques Beaulieu was the first to use the lateral approach for a perineal lithotomy; unfortunately, his method was accompanied by severe morbidity and mortality. 2 Thus, all kinds of conservative measures became quite popular. A variety of plant ingredients were used that resulted in increased urinary volume and reduced pain or that had anti-inflammatory properties.

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Biochemistry of Glycoconjugate Glycans; Carbohydrate-Mediated Interactions

I. Brockhausen , in Comprehensive Glycoscience, 2007

3.03.9.1 α3-Sialyltransferases (ST3Gal)

At least five members of the α3-sialyltransferase (ST3Gal) family (Table 5) may be involved in sialylating the Gal residues of O-glycans. ST3Gal-I and ST3Gal-IV act on the Gal residue of core 1 substrates linked to hydrophobic groups such as benzyl or p-nitrophenyl or peptides. ST3Gal-II,-III, and -VI prefer the N-acetyllactosamine extensions as substrates and are involved in sialyl-Lewisx or sialyl-Lewisa synthesis (Figures 4 and 5). 175

Figure 4. Synthesis of sulfated and sialylated selectin ligands, and Lewisx and Lewisy antigens. Lewisx and Lewisy antigens are found at the termini of type 2 chains and are receptors for selectins. Lewisx is synthesized by the action of α3-Fuc-transferases on N-acetyllactosamine termini (path p). In the synthesis of Lewisy, α2Fuc-transferases FUT1 or FUT2 (path l) act first, followed by α3-Fuc-transferase (path p). 3-Sulfo-Lewisx is synthesized by Gal3ST (path m), followed by α3-Fuc-transferase. The sialyl-Lewisx determinant is synthesized by first adding sialic acid in α2-3-linkage to Gal (path q), followed by α3-Fuc-transferase. Gal-6-O-Sulfotransferase (path r) transfers sulfate to the 6-position of Gal to synthesize 6′-sulfo-sialyl-Lewisx. The 6-O-sulfate group is probably transferred to the terminal GlcNAc residue at an early step (path s), before the addition of Gal (path h). Subsequently, sialic acid and Fuc are added.

Figure 5. Synthesis of Lewisa and Lewisb antigens. Lewisa antigen of mucin-type O-glycans is synthesized by α3/4-Fuc-transferase FUT3 (path t) on type 1 chains. Sialyl-Lewisa and Lewisb structures are assembled by first adding sialic acid or Fucα1-2 residues, respectively, followed by the action of FUT3.

The cloning, structures, and chromosomal locations of sialyltransferase genes have been reviewed. 172,173

Mice lacking the ST3Gal-I gene (Table 6) develop normally but express more unmodified Galβ1-3GlcNAc termini on CD4+ lymphocytes. 176 ST3Gal-IV knockout mice develop bleeding disorders, thrombocytopenia, and a reduction of von Willebrand factor in the serum. 177

Inflammatory conditions in human bronchial mucosal tissue explants are associated with increased α3-sialyltransferase activity toward N-acetyllactosamine, as well as with increased expression of ST3Gal-III and -IV mRNA. 178 In rats, turpentine oil-induced inflammation in the liver caused an upregulation of ST3Gal-I and ST3Gal-III expression. 179

In colorectal carcinomas, the expression of sialyl-Lewisa is also increased. 180 This corresponds to higher mRNA levels for ST3Gal-I, particularly when invasion of lymph vessels is present. 181 In addition, the expression of ST3Gal-IV is increased in poorly differentiated colorectal carcinomas. 182 An increase in α3-sialyltransferase activity and ST3Gal-I mRNA has been observed in breast cancer tissues and cells. 92,183 The increase in α3-sialylation was associated with smaller, truncated, and highly sialylated O-glycans that allowed the exposure of MUC1 mucin epitopes that are normally masked by complex core 2 structures. ST3Gal-I has been localized mainly to the medial- and trans-Golgi compartments of T47D breast cancer cells and normal mammary cells, 88 while C2GnT resides in the cis- and medial-Golgi in these cells. The partial overlap allows the two enzymes to effectively compete for their common core 1 substrates. This was shown by transfection studies with ST3Gal-I and C2GnT1 genes that demonstrated that ST3Gal-I can reduce core 2 formation by increasing sialylation. These two enzymes therefore control overall O-glycosylation, sialylation, branching, and peptide epitope expression of MUC1 mucin. 7

A potent inhibitor of ST3Gal-I, Soyasaponin-I, was found to competitively inhibit the binding of CMP-sialic acid donor substrate. 184 In breast cancer cells MCF-7, the inhibitor stimulated cell adhesion to collagen and Matrigel matrix and decreased cell migration of highly metastatic breast cancer cells, MDA-MB-231, suggesting a role of sialylα2-3Gal-linkages in metastasis.

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