Biomedical subjects

T Osterman

Publications and source records attributed to T Osterman.

At least 19 recordsLinked to original sources

PubMed1998

Effect of clodronate treatment on established bone loss in ovariectomized rats.

The ability of clodronate to prevent bone loss and weakening of bone strength was studied in adult rats with established osteopenia. Six-month-old female Sprague Dawley rats were randomized into 13 groups. One group was killed at the start of the study, nine groups were ovariectomized (ovx), and three groups sham-operated (sham). After 4 months, the ovx rats were given either clodronate or vehicle subcutaneously (s.c.), once a week for 3 or 6 months, the cumulative doses of both dosing regimens being 36, 84, and 300 mg/kg. Clodronate reduced the increase in bone turnover as evidenced by serum osteocalcin and urinary deoxypyridinoline. Cancellous bone loss was more severe in distal femur than in lumbar vertebral body already at 4 months after ovx. Cortical osteopenia of femoral middiaphysis was significant at 7 and 10 months after operation and was in accordance with the impaired bending strength of the femoral shaft. In the tibia, the bending strength was, by contrast, increased at each timepoint after ovx. In distal femur, higher values of cancellous bone volume (BV/TV) were found after 6 months of clodronate treatment than in ovx/vehicle-treated rats. In lumbar vertebrae, only the lowest dose of clodronate slightly counteracted the ovx-induced further decrease in BV/TV, but reduced, at all dosages, the impairment of lumbar vertebral compression strength. The maximum load of femoral neck did not differ between vehicle-treated ovx and sham groups after clodronate treatment, but clodronate reduced the weakening of femoral shaft. A further increase in the bending strength of the tibia was found after clodronate treatment. There was a positive correlation between bending strength and ash weight in both the tibia and the femur. Histomorphometry further showed that long-term use of clodronate does not impair bone mineralization or affect modeling-dependent bone formation. In conclusion, clodronate treatment clearly slows down the progress of bone loss and prevents further weakening of bone strength in femoral shaft and vertebrae, even though it cannot completely reverse the effects of ovariectomy-induced changes in established osteopenia.

Amino Acids↗

PubMed1998

Clodronate prevents osteopenia and loss of trabecular connectivity in estrogen-deficient rats.

Daily oral clodronate treatment was evaluated in Sprague-Dawley rats for its ability to inhibit estrogen-deficiency-induced changes in femoral neck, femoral diaphysis, and lumbar vertebrae (L4-L5). Six-month-old ovariectomized (OVX) rats were administered by gavage a vehicle (Veh) or clodronate (100 or 500 mg/kg/day). Sham-operated (SHAM) control rats received the vehicle (n = 15/group). Treatment was started on the day of operation and continued for 3 months. Trabecular bone volume (BV/TV) and structural variables (trabecular number, Tb.N; thickness, Tb.Th; separation, Tb.Sp; and trabecular bone pattern factor, Tb.Pf) were assessed on secondary spongiosa of the right femoral neck Furthermore, cantilever bending test of the left femoral neck and compression test of L4, ash weight of L5, and morphometric studies of femoral diaphysis were carried out, and serum and urinary markers of bone turnover were determined. The OVX/Veh group had higher levels of serum osteocalcin and alkaline phosphatase and higher urinary excretion of deoxypyridinoline/creatinine than the SHAM/Veh group at 3 months postsurgery, and clodronate reduced these changes. BV/TV of femoral neck, bone mass of L5, and the maximum loads of the femoral neck and L4 were lower after OVX than SHAM operation. Although clodronate prevented trabecular bone loss in the femoral neck and preserved Tb.Pf at the SHAM control level, it failed to preserve the mechanical strength at the femoral neck However, in lumbar vertebrae, clodronate prevented the loss of bone mass and mechanical properties. Furthermore, there was a good positive correlation between maximum load of L4 and the ash weight of L5 (n = 58, r = 0.69, p < 0.001). In the femoral neck (n = 55), Tb.Pf correlated negatively with BV/TV and Tb.N (r = -0.59 and r = -0.55;p < 0.001, respectively) and positively with Tb.Sp (r = 0.61, p < 0.001). In femoral mid-diaphysis, there were no significant changes in cortical bone geometry in any of the groups. We conclude that orally administered clodronate suppresses the enhanced bone turnover in adult OVX rats and preserves trabecular bone volume and connectivity in the femoral neck In the axial skeleton, clodronate has a beneficial effect on lumbar vertebral bone mass and strength.

Administration, Oral↗

PubMed1998

The effect of orally administered clodronate on bone mineral density and bone geometry in ovariectomized rats.

The effects of clodronate administered p.o. on bone mineral density (BMD), bone geometry and strength of bone were investigated in 6-month-old ovariectomized rats. Sixty Sprague-Dawley rats were randomized into four groups. Three groups were ovariectomized (OVX) and one group was sham-operated (SHAM). The OVX groups were given p.o. either clodronate (100 mg/kg/d or 500 mg/kg/d) or a vehicle. The SHAM group received the vehicle. Treatments started on the day of OVX and continued for 3 months. BMD of proximal tibial metaphysis was measured by computed tomography in vivo 1 day before OVX and 6 and 12 weeks after OVX. At the end of the study, left tibiae and femora were removed for ex vivo BMD and bone geometry measurement. A three-point bending test of the tibial shaft was carried out, and ash weights of femur and tibia were determined. OVX induced a marked decrease in total and trabecular BMD over time at the proximal tibial metaphysis. This bone loss was prevented by clodronate. Clodronate also prevented the decrease in BMD and change in bone geometry at distal and proximal femur, as well as the decrease in total ash weight of femur and tibia. OVX did not cause any marked changes in cortical BMD or bone geometry at the level of mid-diaphysis of tibia or femur over a 3-month period. Neither were there any changes between groups in bending strength in the tibial diaphysis. However, a positive correlation (n = 58, r = 0.51, P < .001) was found between bending strength and calculated density-weighted polar moment of resistance of tibial diaphysis. We conclude that clodronate administered p.o. in adult rats prevents changes due to estrogen deficiency in BMD and bone geometry.

Administration, Oral↗

PubMed1997

A comparison of clodronate and indomethacin in the treatment of adjuvant arthritis.

OBJECTIVE AND DESIGN: The therapeutic effects of an anti-resorptive agent, clodronate, were compared with the effects of an anti-inflammatory agent, indomethacin, in rat adjuvant arthritis after therapy and after a follow-up time of two weeks. SUBJECTS: Eighty-one male Lewis rats, 6-7 weeks old, were immunized with heat-killed mycobacteria. TREATMENT: Fourteen days after immunization the animals were treated either with clodronate (50 mg/kg/day, subcutaneously), indomethacin (3 mg/kg/day, orally) or saline (controls) for two weeks. METHODS: Clinical signs of arthritis including the severity of paw swelling were assessed, biochemical variables were measured, and histological features of the non-decalcified tarsus with ankle, intertarsal and tarsometatarsal joints were evaluated for inflammatory soft-tissue, articular, and bone changes. RESULTS: The results indicated that clodronate and indomethacin suppressed significantly the intensity of inflammation, activity of beta-N-acetylglucosaminidase in inflamed hindpaw tissue, serum ICTP (cross-linked carboxyterminal telopeptide of type 1 collagen) level and bone lesions in the tibiotarsal region. The level of serum osteocalcin was also significantly decreased by clodronate. The inhibitory effect of clodronate against arthritic bone changes occurred, however, earlier and was slightly more potent than the effect of indomethacin, while indomethacin was slightly more effective in reducing paw swelling. Both drugs preserved their therapeutic effects during the follow-up time of two weeks. CONCLUSIONS: Clodronate and indomethacin have fairly similar efficacy in suppressing the intensity of joint swelling and preventing bone lesions in adjuvant arthritic rats.

Animals↗

PubMed1997

Clodronate prevents bone loss in aged ovariectomized rats.

The purpose of this study was to investigate the ability of clodronate to prevent ovariectomy (OVX)-induced osteopenia in aged rats. Fourteen-month-old female Sprague-Dawley rats (n = 166) were randomized into six groups. One group was sacrificed at the start of the study, four groups were ovariectomized, and one group was sham-operated (Sham). The OVX rats were given subcutaneously either vehicle (veh) or clodronate at doses of 3, 7, or 25 mg/kg once a week for 3 months, and the Sham rats were given the vehicle. At all dose levels clodronate inhibited trabecular bone loss in the distal femur and in the fourth lumbar vertebral body (L4), and decreased bone resorption as evidenced by urinary deoxypyridinoline excretion. The lowest dose of clodronate preserved serum osteocalcin and endosteal bone formation of secondary spongiosa in L4 at the level of the Sham/veh group. The OVX-induced increase in periosteal bone formation of femoral diaphysis was unaffected by two smaller doses of clodronate, but was decreased to the level of Sham rats after the highest dose. After 3 mg/kg clodronate, the percentage of femoral cortical bone area and the mean relative cortical thickness were higher compared with the OVX/veh group. There was a good positive correlation between the maximum load in three-point bending of the tibia and tibial ash weight. Normal lamellar pattern of newly formed cancellous and cortical bone was found after clodronate treatment. No signs of adverse accumulation of osteoid or any deleterious effect on mechanical strength of long bones and lumbar vertebrae were found.

Aging↗

PubMed1997

Slow-release clodronate in prevention of inflammation and bone loss associated with adjuvant arthritis.

The effects of slow-release calcium clodronate on rat adjuvant arthritis were investigated using two different dosing schedules. In prophylactic treatment, calcium clodronate was given on the same day as the adjuvant injection, and in therapeutic treatment, calcium clodronate administration was delayed until the animals had active disease, to day 14 postadjuvant. Calcium clodronate was given as single i.m. injections into the thigh muscles. Arthritis index, histopathology of hindpaw, quantitative histomorphometry, bone mineral density and serum osteocalcin, alkaline phosphatase and calcium were studied. Calcium clodronate given therapeutically decreased the severity of paw swelling slightly more than prophylactic treatment, a result seen as lower scores of arthritis index. Histopathological evaluation of hindpaws showed that calcium clodronate protected against inflammation-induced bone loss and reactive bone formation in the hindpaw, but not against inflammatory changes involving articular cartilage. Quantitative histomorphometric analysis of the distal femur indicated that trabecular bone area was decreased by 86% in arthritic rats compared with normal untreated controls. Both the prophylactic and the therapeutic treatment with calcium clodronate prevented this osteopenia (P < .001). Bone mineral density measured by computed tomography was also significantly reduced in distal femoral metaphysis in adjuvant arthritic rats, but restoration to virtually normal values occurred with calcium clodronate (P < .001). In both dosing schedules, we observed a suppression of arthritis, which was associated with a decrease in paw swelling and an inhibition of the severe osteopenia in the distal femoral metaphysis. The long duration of action after a single injection of calcium clodronate indicates that the insoluble salt remains at the injection site and is released slowly into the bloodstream.

Alkaline Phosphatase↗

PubMed1997

Distribution of clodronate in the bone of adult rats and its effects on trabecular and cortical bone.

Distribution of clodronate in cancellous and cortical bone of the femur and in cancellous bone of lumbar vertebrae in adult rats was examined by means of quantitative autoradiography. In addition, the effects of clodronate on cancellous and cortical bone were evaluated by bone histomorphometry. Six-month-old male rats were given a mixture of unlabeled and 14C-labeled disodium clodronate subcutaneously on 5 consecutive days at cumulative doses of 125 mg/50 microCi/kg or 250 mg/100 microCi/kg and followed up for 2, 23 or 79 days after the last dose. The highest activity of 14C-clodronate was found in the primary spongiosa of the distal femoral metaphysis and in the cortical bone of the femoral diaphysis. Radioactivity in the lumbar vertebra was found to be about half of that in the femur. No marked decrease in radioactivity was found in bone specimens taken after the follow-ups. In these specimens, however, labeled clodronate originally incorporated into the primary spongiosa was situated further away from the growth plate because of longitudinal bone growth. A cross-section of the femoral shaft showed that incorporation of clodronate was more prominent into the periosteal surface than into the endocortical surface. No marked histological effects were seen, except for an increase in the mineralized hard tissue area in the primary spongiosa of the distal femur.

Animals↗

PubMed1996

Bisphosphonates clodronate and etidronate in the prevention of ovariectomy-induced osteopenia in growing rats.

The aim of this study was to evaluate the ability of the bisphosphonate compounds clodronate and etidronate to prevent ovariectomy-induced bone changes. Three-month-old Sprague-Dawley rats were either ovariectomized (OVX) or sham-operated (SHAM) and further divided into groups receiving either vehicle (n = 30), 25 mg/kg/week of clodronate (n = 25) or 25 mg/kg/week of etidronate (n = 25). The subcutaneous drug administration was started immediately after the surgery and was continued for 12 weeks. OVX rats had accelerated bone turnover rates compared with the SHAM animals, as indicated by the results of dynamic histomorphometry and biochemical markers in serum and urine. Femoral and vertebral mineralized trabecular bone volume and maximum loads in compressions of the femoral neck and lumbar vertebra were lower after OVX compared with the SHAM operation. Both clodronate and etidronate prevented the decrease in trabecular bone volume and suppressed the increase in the bone turnover rate. Clodronate and etidronate also blocked the loss of bone strength in the femoral neck and lumbar vertebra of OVX rats. Both compounds resulted in an absence of double fluorochrome labels on the endocortical surface of the femoral metaphysis, which seemed, however, to be a dose-dependent response. Furthermore, etidronate also lowered serum osteocalcin and diaphyseal endocortical bone formation below the vehicle level both in the OVX and SHAM rats. In conclusion, clodronate and etidronate were effective in preventing the estrogen deficiency-induced decreases in trabecular bone volume and bone strength in rats. Treatment with a high dose of clodronate induced minor signs of abnormally low bone formation but not any impairment of bone mineralization, whereas both of these events were seen with high-dose etidronate administration.

Analysis of Variance↗

PubMed1995

Effect of clodronate on established collagen-induced arthritis in rats.

The collagen-induced arthritis model in rats was used to study the effect of disodium clodronate on inflammation and destruction of tarsal, metatarsal, and interphalangeal bones and joints. Female DA rats were immunized with heterologous type II collagen. Fourteen days after immunization, rats with similar scores were assigned to the different experimental groups. They were treated subcutaneously either with saline (controls) or with clodronate at doses of 12.5 and 25 mg/kg/day five times a week for 2 weeks. Clinical signs of arthritis including the severity of paw swelling were assessed weekly. At the time of killing, histological features of the non-decalcified tarsus with tarsal, tarsometatarsal and interphalangeal joints were assessed for inflammatory soft-tissue, articular, and bone changes. All the arthritic control rats developed severe arthritis as shown by the total histological scores of the hindpaw. The treatment with clodronate (25 mg/kg) decreased clinical signs of arthritis, the activity of the collagen-degrading lysosomal enzyme, beta-N-acetylglucosaminidase, in inflamed hindpaw tissue, serum osteocalcin level and serum cross-linked telopeptide of type I collagen level. Histological evaluation indicated moderate arthritis in 29% of the rats and severe arthritis in 71%. The results show that clodronate given therapeutically to arthritic rats, induced with type II collagen, suppresses the intensity of inflammation and bone lesions in the tibiotarsal and tarsometatarsal regions.

Analgesics, Non-Narcotic↗

PubMed1995

The effects of clodronate on increased bone turnover and bone loss due to ovariectomy in rats.

The present study was carried out to investigate the ability of clodronate to inhibit ovariectomy-induced bone loss and increased bone turnover in rats. Estradiol was administered as a reference compound. Seventy Sprague-Dawley rats were ovariectomized (OVX) or sham-operated (Sham) at the age of 90 days and divided into seven groups. Two Sham and two OVX groups received subcutaneously either the vehicle of clodronate or the vehicle of estradiol. Other OVX groups were given s.c. either disodium clodronate at two dose levels (5 mg/kg or 12.5 mg/kg twice a week) or 17 beta-estradiol (10 micrograms/kg five times a week) for 8 weeks. Femur length, volume, dry weight, and ash weight were determined, and proximal ends of tibiae were used for bone histomorphometry. Markers of bone metabolism were measured from urine and serum. A significant loss of 54% of trabecular bone area of proximal tibial metaphysis was found at 8 weeks after ovariectomy. Clodronate and estradiol inhibited (p < 0.001) this osteopenia. Both drugs prevented the decrease in ash weight/volume of the femur. The inhibitory effect of clodronate and estradiol on bone resorption in OVX rats could be detected also in decreased urinary excretion of hydroxyproline and lysylpyridinoline (p < 0.001). Clodronate and estradiol decreased (p < 0.001) the ovariectomy-induced enhanced tibial endocortical mineral apposition rate (Ec.MAR) on the lateral cortex to the level of the Sham group. In contrast, periosteal MAR analyzed on the medial side of tibial cortical bone did not change significantly in the OVX/Veh group. Estradiol decreased periosteal MAR to below the level in the Sham group (p < 0.01). These results suggest that ovariectomy of growing rats resulted in tibial and femoral osteopenia two months later. Clodronate as well as estradiol can suppress bone resorption and turnover in ovariectomized rats, inhibiting the development of osteopenia. Both clodronate doses (5 and 12.5 mg/kg) had beneficial effects in ovariectomized animals.

Analgesics, Non-Narcotic↗

PubMed1994

Effect of clodronate on established adjuvant arthritis.

The rat adjuvant arthritis model was used to study the effect of disodium clodronate on inflammation and destruction of tarsal bones and joints. Male Lewis rats were given an intradermal injection of mycobacteria. Fourteen days after immunization, rats with similar scores were assigned to the different experimental groups. They were treated subcutaneously either with saline (controls) or with clodronate at doses of 12.5 and 25 mg/kg/day five times a week for 2 weeks. Clinical signs of arthritis including the severity of paw swelling were assessed weekly. At the time of sacrifice, histological features of the non-decalcified tarsus with ankle, intertarsal and tarsometatarsal joints were assessed for inflammatory soft-tissue, articular and bone changes. The total histological score of the hindpaw indicated that 58% of the control rats developed moderate arthritis and 42%, severe arthritis. The treatment with clodronate (25 mg/kg) decreased clinical signs of arthritis and the activity of the collagen-degrading lysosomal enzyme, beta-N-acetylglucosaminidase, in inflamed hindpaw tissue. Histological evaluation indicated moderate arthritis in 83%, but no severe arthritis. The lower dose of clodronate also decreased the severity of the disease; the decrease was, however, statistically insignificant. The results show that clodronate given therapeutically to adjuvant arthritic rats suppresses the intensity of the inflammation and prevents secondary articular and bone lesions in the tibiotarsal region.

Animals↗

PubMed1991

Pharmacokinetics of clodronate after single intravenous, intramuscular and subcutaneous injections in rats.

The pharmacokinetics of clodronate was studied in rats after single intravenous, intramuscular and subcutaneous doses of a mixture of unlabelled and 14C-labelled disodium clodronate (25 mg/5 muCi/kg). The peak clodronate concentration in plasma was reached within 5 min., and the drug was eliminated with a half-life of about 1.5 hr regardless of administration route. Bioavailabilities after intramuscular and subcutaneous administration were 105% and 89%, respectively. During the 72 hr collection period, the mean share of clodronate recovered from the urine was about 53% of the dose regardless of administration route. Most of the drug was excreted during the first 24 hr. The amount of clodronate in bone (femur) was 186 micrograms/g tissue at 2 hr after intravenous administration, 188 micrograms/g after intramuscular administration and 157 micrograms/g after subcutaneous administration. It is concluded that absorption of clodronate after intramuscular and subcutaneous administration is rapid and good, and that the concentrations of the drug in bone after 2 hr are about the same as after intravenous administration.

Absorption↗

PubMed1991

Level of clodronate in bone after single and repeated subcutaneous injections in rats.

The levels of clodronate in bone and plasma were determined in rats after subcutaneous injection of a mixture of unlabelled and 14C-labelled disodium clodronate as a single dose (25 mg/5 muCi/kg or of 125 mg/25 muCi/kg), and as repeated doses (25 mg/5 muCi/kg) once or five times a week for five weeks. The level of clodronate in bone increased dose-dependently. However, during repeated administration some saturation in bone was observed. The accumulation of clodronate in femur was higher than in ankle. No clear differences in concentration of clodronate in bone could be seen after different dosage schedules when the total doses were the same.

Absorption↗

PubMed1989

Inflammation-related changes in cyclic AMP and cyclic GMP in bovine mastitis.

Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) concentrations in milk and plasma samples from healthy and mastitic cows were determined by radioimmunoassay and compared with prostaglandins (PGE2, PGF2 alpha and thromboxane B2 [TXB2]), phospholipids and other relevant parameters in milk and blood. The concentrations of cAMP were about five times higher in plasma (p less than 0.01) than in milk, whereas the cGMP concentration in milk was three times higher (p less than 0.01) than that in plasma in both healthy and diseased animals. In mastitic milk, the cAMP and cGMP concentrations were 19% and 65% and in blood plasma 13% and 84% higher respectively than in healthy animals. In milk, cyclic nucleotide concentrations correlated with the markedly elevated cell count and also with the prostaglandin concentration and pH. In blood, cAMP correlated positively with phospholipids and cGMP with reduced glutathione (GSH). These changes are considered to be important in the disease process and, in particular, the increase in cGMP deserves further study.

Animals↗

PubMed1989

Free fatty acids and lipid peroxidation in normal and mastitic bovine milk.

Milk levels of free fatty acids (FFA) and prostaglandins (PGs) were determined in healthy cows and in those with mastitis and compared with some parameters commonly used for diagnosing mastitis. A modified gas chromatography-mass spectrometry method was used. In mastitis there was a substantial overall increase in FFA levels in milk. Specific attention was paid to the fate of the long-chain polyunsaturated fatty acids, known as precursors for the production of PGs, leukotrienes and other eicosanoids. Both the omega-6 and omega-3 lines of these lipids were increased in mastitis, but only in proportion to other FFA. The milk levels of PGs (PGF2, PGF2 alpha, thromboxane B2) were elevated in the same proportion. The possible importance of lipid peroxidation, inflammatory reaction and host defence are evaluated in relation to tissue destruction and oxidative killing of pathogens. It may be possible to manipulate the intake and fate of FFA in the organism by dietary intake, antioxidants and proper storing of feed. It is concluded that in studies concerning FFA special attention should be given to those long-chain fatty acids that are precursors for the formation of eicosanoids.

Animals↗

PubMed1989

Role of plasma fatty acids, prostaglandins and antioxidant balance in bovine mastitis.

Plasma levels of free fatty acids (FFA) were measured in cows with mastitis. FFA levels are known to be elevated in milk of affected cows, and similar increases were now observed in blood plasma. Of the long-chain polyunsaturated fatty acids which serve as precursors for prostaglandins (PGs), leukotrienes (LT) and related eicosanoids, arachidonic acid (C20: 4 omega-6) was elevated by 156 per cent and C20: 3 (consisting of both omega-3 and omega-6) 153 per cent; eicosapentaenoic acid (20: 5 omega-3), not present in the plasma of healthy animals, was detected in blood of mastitic animals. Arachidonic acid correlated positively with the plasma levels of PGs. Total plasma phospholipids were increased as well, and they were positively correlated with the levels of linoleic and arachidonic acids. Changes in FFA levels correlated positively with parameters of inflammation, like bovine serum albumin and serum N-acetyl-beta-D-glucosaminidase, but negatively with the antioxidant status of the animals (vitamin E, glutathione peroxidase). As PGs and LTs are mediators of inflammation, and products of lipid peroxidation, the increase of plasma FFA could be related to tissue damage caused by oxygen free radicals. Similar processes are, however, involved also in host defence, e.g. in oxidative killing of pathogens.

Acetylglucosaminidase↗

PubMed1987

Milk prostaglandins and electrical conductivity in bovine mastitis.

Prostaglandin (PG) levels in milk samples from healthy and mastitic cows were determined by radioimmunoassay. In composite milk the PG levels were rather high both in healthy and mastitic samples, and the only significant difference was in thromboxane B2 (TXB). In quarter milk samples classified according to the degree of mastitis by use of somatic cell counts, PGE2 was 40, PGF2 alpha 15, and TXB2 44 per cent higher respectively in affected samples. PG levels were in good correlation with somatic cell counts (r = 0.63-0.68, p less than 0.01) and electrical conductivity (r = 0.36-0.52, p less than 0.01), two established criteria for diagnosis of mastitis. PGE2 also correlated with protein, TXB2 with fat content. PGF 2 alpha was in a negative correlation with milk yield. The good correlation of PGs with somatic cell counts and electrical conductivity suggests that PGs might be used as markers of mastitic inflammation.

Animals↗

PubMed1986

Prostaglandins and glutathione peroxidase in bovine mastitis.

Prostaglandin (PG) levels in milk and plasma samples from mastitic cows were determined by radioimmunoassay and compared with erythrocyte glutathione peroxidase (GSH-Px) and other relevant parameters in milk and blood. The overall levels of PGE2, PGF2 alpha and thromboxane B2 (TXB2) in milk were two to four times higher than in blood plasma both in healthy and diseased animals (P less than 0.01). In mastitic milk the PG levels were 24 to 55 per cent and in blood plasma 41 to 95 per cent higher than in healthy animals. The changes were significant and largest for the PGF2 alpha values. In milk, the PG concentrations correlated with the markedly elevated cell count (r = 0.49 to 0.57), and TXB2 values also correlated with milk yield. In blood, PGE2 and PGF2 alpha correlated positively with serum albumin, and PGE2 also correlated with glutathione (GSH). PGE2 and PGF2 alpha correlated negatively with GSH-Px and gamma-glutamyl transferase. The substantial decline in GSH-Px in mastitic animals (P less than 0.01) may be related to changes in lipid peroxidation and PG formation. The possible implications of these findings in the treatment of mastitis are discussed.

Animals↗