Effect of urban ozone levels on laboratory-induced respiratory infections

The effect of the time of exposure to an aerosol of viable microorganisms on the incidence of respiratory infections associated with a 3 h exposure to ozone (O₃) was studied. The 157 and 196 $\text{μg}\text{m}{}^3$ (0.08–0.1 ppm) levels of O₃ used occur regularly in some urban communities. The studies reported here show that the susceptibility of mice to a laboratory-induced infection can be maximally enhanced if the infectious challenge is concurrent with the exposure to O₃.     

Effects of exposure to ozone on susceptibility to experimental tuberculosis

Exposure of mice to 1.96 $\text{mg}\text{m}{}^3$ ozone (O₃) 3 $\text{h}\text{day}$, 5 days/week, for up to 8 weeks beginning at 1 or 2 weeks after challenge with Mycobacterium tuberculosis R 1Rv resulted in significant enhancement of bacterial titers in the lungs at 5 through 8 weeks after challenge when compared to mice exposed to filtered air. Exposure to lower concentrations of O₃ did not produce any significant changes compared to controls.Exposure of guinea pigs to 2.9 $\text{mg}\text{m}{}^3$ O₃ for 3 h immediately after challenge with M. tuberculosis resulted in a suppression of the cutaneous delayed hypersensitivity response, without affecting the serum hemagglutination antibody titers. However, exposure of guinea pigs to 0.98 $\text{mg}\text{m}{}^3$ O³ 3 $\text{h}\text{day}$ for 5 days, initiated within 3 h after the infectious challenge, enhanced hemagglutination antibody titers initially, but the delayed hypersensitivity reaction did not differ from controls.     

Carbon disulphide tetratogenicity and postnatal effects in rat

Pregnant albino rats were exposed to carbon disulphide vapour in concentrations of 50, 100 or 200 $\text{mg}\text{m}{}^3$throughout gestation. Two successive generations (F₁ and F₂) were studied.Concentration levels of 100 and 200 $\text{mg}\text{m}{}^3$ produced marked dose-related impairment in the prenatal development of the F₁ progeny, with increase of early embryonal lethality, reduction in foetal weight and a high incidence of malformations affecting mostly the brain and limbs. Postnatal viability, body weight, lipid and energy metabolism and behaviour were also impaired. Behavioral deviations were observed even at 50 $\text{mg}\text{m}{}^3$.After reaching sexual maturity the F₁ rats were mated within their experimental groups, but no further carbon disulphide exposure was applied. The adverse effects on progeny were still detectable in the F₂ generation. Structural abnormalities of the same type as those found in the F₁ at 100 and 200 $\text{mg}\text{m}{}^3$ exposure were observed in their progeny and, postnatally, statistically significant behavioral changes were observed in the progeny of all test groups.     

Influence of dietary polybrominated biphenyl on antibody and host defense responses in mice

Male $\text{Balb}\text{cByJ}$ mice were fed diets containing 5 or 167 ppm of polybrominated biphenyls (PBB) (Firemaster, FFl, lot No. 7042) for either 3 or 6 weeks and then evaluated for their ability to produce antibody and to resist a challenge with malaria or endotoxin. Animals which received a dietary exposure of either 5 or 167 ppm of PBB for 3 or 6 weeks manifested no alteration in their resistance to a challenge infection with Plasmodium berghei (NYU-2), a lethal murine malaria parasite. However, mice which were fed a diet containing 167 ppm of PBB for 3 or 6 weeks had a significant increase in endotoxin (LPS) sensitivity while no change in LPS sensitivity was observed in mice fed 5 ppm of PBB. Peak primary antibody production to sheep erythrocytes, expressed as $\text{PFC}\text{10}{}^{\mathrm{<mtext>6</mtext>}}$ spleen cells, was reduced almost 50% in mice fed a diet containing 167 ppm for 3 weeks, however, no change in $\text{PFC}\text{10}{}^{\mathrm{<mtext>6</mtext>}}$ cells was observed at 6 weeks. A dietary level of 5 ppm of PBB did not alter primary antibody formation at either 3 or 6 weeks. The peak secondary PFC response in both 5- and 167-ppm-treated groups was delayed by 1 day, relative to control values. $\text{PFC}\text{10}{}^{\mathrm{<mtext>6</mtext>}}$ cells, measured on the day of the peak control response, were depressed 60% at 3 weeks and over 85% at 6 weeks at both doses. Serum IgM levels in the mice receiving 167 ppm of PBB were reduced 23–63% during the I° and II° responses, serum IgG was only moderately reduced and serum IgA was unaltered throughout the study. These results suggest that PBB has a minimal effect on antibody production to T-dependent antigens or on host defense to protozoan parasites yet causes a selective depletion of serum immunoglobulin isotypes. The marked increase in LPS sensitivity suggests a compromised macrophage detoxification capability.     

Kinetic studies on the deethylation of ethoxybenzamide: A comparative study with isolated hepatocytes and liver microsomes of rat

Kinetic parameters (K_m and V_max) of ethoxybenzamide deethylation in isolated rat hepatocytes and liver microsomes were compared. Adjustment of cofactors in microsomal deethylation, such as NADPH and Mg²⁺, to give optimum conditions, and appropriate correction of the apparent kinetic parameters for nonspecific binding and microsomal yield resulted in good agreement among the kinetic parameters of isolated hepatocytes [$\text{V}{}_{\mathrm{<mtext>max</mtext>}}\text{= 0.0863 μmole · min}{}^{\mathrm{?1}}\text{· (g liver)}{}^{\mathrm{?1}}$ and K_m = 0.459 mM] and microsomes [V_max = 0.124 μmoles · min^?1 · (gliver)^?1 and K_m = 0.378 mM].     

Concentrations of nitrate in normal human urine and the effect of nitrate ingestion

A method suitable for the analysis of nitrate in human urine was developed. Normal urinary concentrations of nitrate in urine of human volunteers in Dade County, Florida, where the drinking water contains negligible amounts of nitrate, averaged 47.6 ppm of $\text{NO}{}_3{}^{\mathrm{?}}$ (SD = 17.3). On a vegetable and preserved-meat-free diet, the nitrate concentration was reduced (10 to 30 ppm of $\text{NO}{}_3{}^{\mathrm{?}}$), but, on nitrate-supplemented drinking water, the urinary concentration rose to a range of 34–87 ppm of $\text{NO}{}_3{}^{\mathrm{?}}$. A high vegetable diet resulted in peak urinary nitrate concentrations of 270–425 ppm. These results indicated that nitrate in drinking water is a factor in determining urinary nitrate concentration, but that vegetable ingestion is of greater significance.     

Tissue distribution of histamine in a mutant mouse deficient in mast cells: Clear evidence for the presence of non-mast-cell histamine

The contents of histamine in various tissues of mutant mice deficient in mast cells ($\text{W}\text{W}{}^{\mathrm{v}}$) and in congenic normal mice (+/+) were determined by high-performance liquid chromatography and were compared. In spite of the absence of mast cells in $\text{W}\text{W}{}^{\mathrm{v}}$ mice, the histamine content of their whole bodies was about 5–10% of that of +/+ mice. The skin, heart and lungs of $\text{W}\text{W}{}^{\mathrm{v}}$ mice contained negligible amounts of histamine (about 2% of that in +/+ mice), but the liver, kidneys and spleen contained appreciable histamine (8–15% of that in +/+ mice), and the brain and stomach contained much histamine (45 and 34%, respectively, of that in +/+ mice). These results indicate the presence of non-mast-cell histamine, especially in the brain and stomach, where it may play important physiological roles.     

Mechanisms by which quipazine,a putative serotonin receptor agonist,alters brain 5-hydroxyindole metabolism

Quipazine (2-[1-piperazinyl] quinoline maleate) was shown to increase serotonin and decrease 5-hydroxyindoleacetic acid concentrations in whole brain, several brain regions, and the spinal cord of rats 1 hr after its administration (10 mg/kg, i.p.). In animals with transected spinal cords, quipazine induced stronger activation of extensor reflexes than 5-hydroxytryptophan, chlorimipramine, or Lilly 110140. This response could be blocked by methiothepin. In slices of rat cerebral cortex, quipazine inhibited the uptakes of [³H]-serotonin (EC₅₀ = 10^?6 M) and [³H]-norepinephrine ($\text{EC}{}_{50}\text{= 2 × 10}{}^{\mathrm{?6}}\text{m}$); it was equipotent with Lilly 110140 in inhibiting serotonin uptake, but less potent than chlorimipramine ($\text{EC}{}_{50}\text{= 10}{}^{\mathrm{?7}}\text{m}$). Quipazine administration to rats did not inhibit monoamine oxidase activity, and actually elevated brain tryptophan levels. These observations suggest that the effects of quipazine on brain serotonin and 5-hydroxyindoleacetic acid concentrations could have been caused by direct activation of central serotonin receptors (which would secondarily decrease impulse flow along serotonergic neurones), or by the inhibition of serotonin reuptake, or by both mechanisms.     

Studies on the respiratory uptake and excretion and the skin absorption of methyl n-butyl ketone in humans and dogs

Methyl n-butyl ketone (MnBK) has produced peripheral neuropathy in experimental animals and is implicated in an occupationally produced neuropathy. Since occupational exposure to MnBK is by inhalation or skin contact, both the absorption and elimination of MnBK vapor and its absorption through skin were investigated. Studies were carried out first with male beagle dogs and subsequently with human volunteers. Humans exposed for 7.5 hours to 10 or 50 ppm or for 4 hr to 100 ppm of MnBK vapor absorbed between 75 and 92% of the inhaled vapor. Unchanged MnBK was not eliminated extensively in the postexposure breath or in urine. 2,5-Hexanedione, a metabolite of MnBK known to be neurotoxic in rats, was found in the serum of humans exposed to either 50 or 100 ppm of MnBK. The absorption and elimination of MnBK in dogs was similar to that observed in humans. The skin absorption of [1-¹⁴C]MnBK or a $\text{9}\text{1}$ ($\text{v}\text{v}$) mixture of methyl ethyl ketone $\text{(MEK)}\text{[1-}{}^{14}\text{C]MnBK}$ was determined by excretion analysis. Two volunteers exposed by skin contact to [1-¹⁴C]MnBK absorbed 4.8 μg min^?1 cm^?2 and 8.0 μg min^?1 cm^?2, respectively. Skin exposure to $\text{MEK}\text{[1-}{}^{14}\text{C]MnBK}$ resulted in the respective absorption of 4.2 and 5.6 μg min^?1 cm^?2 by two individuals. Two volunteers given an oral dose of [1-¹⁴C]MnBK (2 μCi; 0.1 mg/kg) excreted 49.9 and 29.0% of the dose, respectively, as respiratory ¹⁴CO₂ within 3 to 5 days and 27.6 and 25.0% of the dose, respectively, in urine within 8 days. Both [1-¹⁴C]MnBK and $\text{MEK}\text{[1-}{}^{14}\text{C]MnBK}$ were absorbed through the skin of dogs. These findings show that MnBK is readily absorbed by the lungs, the gastrointestinal tract, and through the skin, is not eliminated extensively unchanged in breath or urine, and is metabolized to CO₂ and 2,5-hexanedione. Radioactivity derived from [1-¹⁴C]MnBK was excreted slowly by man, suggesting that repeated daily exposure to high concentrations of MnBK may lead to a prolonged exposure to neurotoxic metabolites.     

Inhalation studies on the biotransformation and elimination of [14C] trichlorofluoromethane and [14C] dichlorodifluoromethane in beagles

The possible biotransformation of trichlorofluoromethane (FC-11) and dichlorodifluoromethane (FC-12) was investigated in 4 male and 2 female adult Beagles after a short (6- to 20-min) inhalation. Dogs were anesthetized with ketamine and succinylcholine, intubated, and ventilated artificially. Trichlorofluoromethane (1000–5000 ppm, $\text{v}\text{v}$) or dichlorodifluoromethane 38000–12,000 ppm, $\text{v}\text{v}$) containing up to 180μ Ci of $\text{[}{}^{14}\text{C}\text{]}\text{fluorocarbon}$ was delivered from 110-liter Teflon bags, and all exhalations were collected via a nonrebreathing valve in similar bags for 1 hr. Venous blood samples were withdrawn at appropriate times and assayed for fluorocarbon-associated radioactivity. Exhalation bags were assayed for $\text{[}{}^{14}\text{C}\text{]}\text{fluorocarbon}$ and ¹⁴CO₂. Urine was collected for up to 3 days and assayed for ${}^{14}\text{C}$ metabolites as nonvolatile radioactivity. In some experiments animals were sacrificed 24 hr after exposure and tissues were removed for determination of nonvolatile radioactivity. Essentially all of the administered (inhaled) fluorocarbon was recovered in the exhaled air within 1 hr. Only traces of radioactivity were found in urine or exhaled carbon dioxide. All tissues contained measurable concentrations of nonvolatile radioactivity 24 hr after exposure but together represented less than 1% of the administered dose. It is not possible to determine if these trace levels are associated with metabolites of the fluorocarbons or with the unavoidable radiolabeled impurities present in the administered gas mixture. Neither phenobarbital pretreatment (60 mg/day for 3 days) nor prolonged exposure (50–90 min) produced any alteration of these results. Thus, it can be concluded that FC-11 and FC-12 are relatively refractory to biotransformation after a short inhalation exposure and that they are rapidly exhaled in their unaltered chemical form.     

Nitrate formation in rats exposed to nitrogen dioxide

Sprague-Dawley rats exposed to atmospheres containing low levels of nitrogen dioxide (NO₂) for 24 hr had increased levels of nitrate in their urine on the day of exposure and on the 3 subsequent days. The total increase in urinary nitrate was linearly related to the nitrogen dioxide concentration administered. We recovered in urine 8.4 ± 1.1 μmol nitrate/ppm $\text{NO}{}_2\text{24}\text{-hr}$ exposure (slope ± 95% confidence limits) for 185-g rats. Both the linearity and magnitude of this effect imply that reaction with respiratory tract water is not a major pathway of NO₂ absorption in the lung. Instead, our observations support the hypothesis that the major interaction of NO₂ in the lung is with readily oxidizable tissue components to form nitrite. We estimate that 9.6 μmol of nitrite is formed in the respiratory tract of the rat per ppm NO₂ per 24-hr exposure. We also estimate that humans breathing air containing 0.1 ppm NO₂ have about 3.6 mg of nitrite formed in their respiratory tract per day.     

Effect of polychlorinated biphenyls on the immune responses of rhesus monkeys and mice.

The relationship between lipid peroxidation, glutathione (GSH) content, and CCl₄-induced toxicity was investigated in rat hepatocytes isolated by a collagenase-perfusion technique. Two chemical initiators of lipid peroxidation, ferric ions complexed with adenosine diphosphate ($\text{ADP}\text{Fe}{}^{\mathrm{3+}}$) and diethyl maleate, were studied for comparison. CCl₄ caused a reduction of intracellular K⁺ and release of alanine aminotransferase (ALT) into the medium, but no evidence of lipid peroxidation, as measured by the absorbance of thiobarbituric acid (TBA)-reacting materials and lipid-extract diene conjugation. $\text{ADP}\text{Fe}{}^{\mathrm{3+}}$ caused lipid peroxidation, but only a small loss of K⁺. Diethyl maleate caused a greater amount of lipid peroxidation and cell damage than did $\text{ADP}\text{Fe}{}^{\mathrm{3+}}$. Neither response appeared to be related to the GSH content, which was reduced by diethyl maleate, but not by $\text{ADP}\text{Fe}{}^{\mathrm{3+}}$, and by CCl₄ only at the highest dose. The results suggest that lipid peroxidation is not a requisite step in CCl₄-induced toxicity in isolated hepatocytes.     

The effects of cadmium, manganese and aluminium on sodium-potassium-activated and magnesium-activated adenosine triphosphatase activity and choline uptake in rat brain synaptosomes

The effects of Cd²⁺, Mn²⁺ and Al³⁺ on rat brain synaptosomal sodium-potassium-activated and magnesium-activated adenosine triphosphatase (Na-K-ATPase and Mg-ATPase) activity and choline uptake were studied. All three types of metal ions inhibited Na-K-ATPase activity more markedly than Mg-ATPase activity. The rank order of inhibition of Na-K-ATPase was: $\text{Cd}{}^{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 5.4 μ}\text{M}\text{) >}\text{Mn}{}_{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 955 μ}\text{m}\text{) >}\text{Al}{}^{\mathrm{3+}}\text{(}\text{ic}{}_{50}\text{= 8.3}\text{mM}$). The rank order of inhibition of Mg- was:$\text{Cd}{}^{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 316 μ}\text{M}\text{>}\text{Mn}{}^{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 5.5}\text{mM}\text{>}\text{Al}{}^{\mathrm{3+}}\text{(}\text{ic}{}_{50}\text{= 21.9}\text{mM}\text{).}\text{Al}{}^{\mathrm{3+}}$ was most potent in inhibiting synaptosomal choline uptake ($\text{ic}{}_{50}\text{= 24μ}\text{M}$ in the absence of Ca²⁺ and 123 μ.M in the presence of 1 mM Ca²⁺). $\text{Cd}{}^{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 363 μ}\text{M}\text{)}$ was a more effective inhibitor of choline uptake than $\text{Mn}{}^{\mathrm{2+}}\text{(}\text{ic}{}_{50}\text{= 1.2?1.5}\text{mM}\text{)}$ . The presence of 1 mM Ca²⁺ did not alter choline uptake, nor did it antagonize the inhibitory actions of the three metals. Our observations that Cd²⁺ and Al³⁺ inhibited synaptosomal choline uptake, but did not show parallel inhibitory effects on Na-K-ATPase activity directly contradicts the ionic gradient hypothesis. These results are also discussed in relation to the in vivo neurotoxicity of cadmium, manganese and aluminium.     

Early damage indicators in the lung. III. Biochemical and cytological response of the lung to inhaled metals salts.

The validity of using the enzymatic and cytologic profile of airway fluids to indicate lung damage was tested in animals exposed by inhalation to either a known toxic metallic salt (CdCl₂) or a relatively innocuous salt (CrCl₃). The enzymatic and cytologic response of the airways was compared to histopathological evaluation of lung damage. Syrian hamsters were exposed to an aerosol of CdCl₂ (aerodynamic diameter = 1.7 μm, $\text{σ}{}_{\mathrm{g}}\text{? 1.7}$) to achieve an initial lung burden (ILB) of 0.6 ± 0.3 and 4.4 ± 1.2 μg of CdCl₂ or to an aerosol of CrCl₃ (count median diameter = 1.2 μm, $\text{σ}{}_{\mathrm{g}}\text{? 1.5}$) to achieve an ILB of 0.7 ± 0.2 or 20 ± 10 μg of CrCl₃. Animals were sacrificed at 2 hr, 1, 7, and 21 days after exposure. A sample of airay fluid was obtained by bronchopulmonary lavage and examined for the enzymatic profile of the cell-free fraction and the cytological profile of the cell fraction. Lung tissue enzyme activities were also measured and histopathologic evaluations were made on lung tissue from exposed, but nonlavaged, animals. In the lavage fluid from animals exposed to CdCl₂, the enzymatic and cytologic data demonstrated a dose-response pattern and the airway response preceded enzymatic changes in the lung tissue. Tissue morphological changes correlated well with the biochemical changes. The response of the lung to CrCl₃ was minimal by both morphological and biochemical evaluations. Airway enzymatic and cytologic responses were shown to be potentially useful as indicators of lung damage in toxicological screening programs.     

Similar activities of nerve growth factor and its homologue proinsulin in intracellular hydrogen peroxide production and metabolism in adipocytes: Transmembrane signalling relative to insulin-mimicking cellular effects

Generation of hydrogen peroxide in adipocyte plasma membrane and its intracellular metabolism and regulatory role have been shown by Mukherjee and co-workers to be a major effector system for insulin [Fedn Proc.35, 1694 (1976); Archs Biochem. Biophys.184, 69 (1977); Biochem. Pharmac.27, 2589 (1978); Fedn Proc.37, 1689 (1978); and Biochem. Pharmac.29, 1239 (1980)]. The possible involvement of this mechanism in the action of structurally similar polypeptides having some insulin-like metabolic effects was investigated. The β-subunit of nerve growth factor (2.5 S NGF, mol. wt 13,500) which has a striking structural homology with proinsulin and has been reported to exert certain insulin-like metabolic effects in its own target tissues (e.g. growing neurites and sympathetic ganglia), and the insulin-derived polypeptides, desalanine-insulin and desoctapeptide-insulin, as well as proinsulin, were examined for their effects on rat adipocytes, employing the technique of formate oxidation. Both NGF and proinsulin caused increased [¹⁴C]formate oxidation, showing similar intrinsic activities, up to a maximum of 140–160% of the basal rate; insulin increased the rate to 190–210% of the basal rate. The relative potencies of the hormones toward H₂O₂ formation and stimulation of the pentose phosphate pathway activity were: insulin $\text{(}\text{EC}{}_{50}\text{: 2.5 × 10}{}^{\mathrm{?11}}\text{M}\text{)}$, desalanine-insulin $\text{(}\text{EC}{}_{50}\text{: 2.5 × 10}{}^{\mathrm{?10}}\text{M}\text{)}$ , proinsulin $\text{(}\text{EC}{}_{50}\text{: 8 × 10}{}^{\mathrm{?9}}\text{M}\text{)}$, and NGF $\text{(}\text{EC}{}_{50}\text{: 10}{}^{\mathrm{?9}}\text{M}\text{)}$. The biologically inactive derivative, desoctapeptide-insulin, did not stimulate glucose oxidation, although it caused a small increase in formate oxidation, with an $\text{EC}{}_{50}\text{of}\text{5 × 10}{}^{\mathrm{?7}}\text{M}$, indicating a suboptimal level of H₂O₂ formation in the elevation of the hexose monophosphate shunt activity. 3-Amino-1,2,4,-triazole (50 mM), which irreversibly decomposes the peroxidatic compound II of the catalase: H₂O₂ complex, inhibited formate oxidation to a greater extent in the hormone-treated cells than in the control cells, whereas sodium azide, an inhibitor of the hemoprotein, catalase, completely inhibited it. The abilities of the polypeptides to stimulate H₂O₂ formation correlated with their abilities to promote lipogenesis from [U-¹⁴C]-D-glucose, as expected of insulin. The cellular GSH/GSSG ratio increased concomitantly with the stimulation of glucose oxidation via the shunt, indicating a tight coupling between these processes. The results confirm that the hydrogen peroxide production is a common basis of the metabolic actions of growth-promoting polypeptide hormones or mitogens beyond their respective receptors.     

Effect of stannous chloride on rat femur

Oral administration of stannous chloride (SnCl₂) (1.0 mg $\text{Sn}{}^{\mathrm{2+}}\text{kg}$ body weight) to rats, twice daily for 30 or 90 days, caused a significant decrease of the calcium (Ca) content and acid phosphatase activity of the femoral epiphysis but did not reduce those of the femoral diaphysis. 1.0 mg $\text{Sn}{}^{\mathrm{2+}}\text{kg}$ for 30 days produced a significant decrease of alkaline phosphatase activity of the femoral epiphysis, but did not lower that of the femoral diaphysis. The results indicate that Sn may inhibit bone formation directly in the femoral epiphysis of rats.     

Kinetic studies on the metabolism of ethylmorphine by isolated hepatocytes from adult rats

Hepatocytes of adult rats were isolated by infusion of a hyaluronidase collagenase mixture. High yields of cells excluding trypan blue were obtained. These cells, in Hank's buffer containing rat serum and 0.1% glucose, $\text{N-}\text{demethylate}\text{[}{}^3\text{H-CH}{}_3\text{-N]}$ethylmorphine. The formaldehyde initially formed is further metabolized to tritiated water. Fifteen per cent of the original metabolic activity was observed after 21 hr at 37° in 5% CO₂-air, and cumulative metabolism is linear for up to 90 min under these conditions. The K_m for the N-demethylation of [³H-CH₃-N]ethylmorphine is 50 μM, 20 per cent of the value observed for this reaction by musomal preparations. An active transport of the substrate into the cell is postulated to account for this difference.     

Biological fate of a representative lipophilic metal compound (ferrocene) deposited by inhalation in the respiratory tract of rats

Rats were exposed by the nose-only route to ferrocene vapor labeled with ${}^{59}\text{Fe}$ and tritium. Serial sacrifices were performed up to 117 days following exposure. Over 75% of the tritium label was excreted within the firt day but the ⁵⁹Fe label largely remained in the bronchopulmonary and nasopharyngeal regions over the duration of the experiment.     

The role of lipid,free radical initiator,and oxygen on the kinetics of lipid peroxidation

The relationship between the concentration of unsaturated lipid, free radical initiator, and oxygen concentration on the kinetics of lipid peroxidation was determined. The rate of lipid peroxidation was studied with the thiobarbituric acid (TBA), diene conjugation (DC), and ferrithiocyanate (Fe-SCN) methods. The rate of peroxidation was half-order with respect to unsaturated lipid, initiator, and oxygen. The half-order relationship could be expressed as: $\text{rate}\text{= (}\text{fk}{}_1\text{k}{}_2\text{k}{}_3\text{k}{}_6{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}\text{(}\text{azobisisobutyronitrile}\text{)}{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}$$\text{(}\text{RH}{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}\text{(}\text{O}{}_2\text{)}{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}$. The half-order relationship was found with linoleic (18:2), linolenic (18:3), and arachidonic (20:4) acids. A linear relationship existed between the logarithm of unsaturation and the rate of peroxidation. No peroxidation of linolenic acid was indicated when the DC method was employed, but was when the TBA and Fe-SCN methods were used.