The effects of ethylene chlorohydrin on fatty acid synthesis 1 2 3

Abstract

Male chicks weighing 700 to 900 g. received an acute or eight doses IG of 60 or 40 mg/kg ethylene chlorohydrin (ECH) respectively and were sacrificed eighteen hours after the last dose. Mitochondrial elongation of fatty acids was decreased significantly while fatty acid synthetase activity was not significantly affected by ECH treatment. Cytochrome c oxidase activity in fresh whole liver homogenate was significantly higher in chicks subjected to acute exposure with ECH when compared to the controls. Upon freezing and thawing of homogenates, cytochrome c oxidase activity increased significantly in the control group but was unchanged in the ECH group which suggests that the mitochondrial membrane integrity is compromised by the ECH treatment. Serum and liver triglyceride levels were significantly elevated in both the single and multiple ECH dose groups. Liver to body weight ratios were significantly higher in both treatment groups when compared to their controls. Histological examination of the liver of ECH‐treated chicks showed cytoplasmic clearing of the cells but no vacuolization or centri‐lobular necrosis. Serum isocitrate dehydrogenase levels were significantly higher in the multiple treatment ECH group than in the control group.     

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on serum insulin and glucose levels in the rabbit

Serum insulin and glucose were measured in young male rabbits after a single intraperitoneal dose of 1 or 50 micrograms/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Serum insulin levels in the high dosed rabbits were significantly decreased between 15 min and 8 h post treatment, equivalent after 24 h, significantly elevated 48 h post treatment, and they were not different at 10 days post-treatment when compared to weight matched and pair-fed controls. At the low dose, rabbits showed no differences in serum insulin from controls. In the high dose group, serum glucose levels were generally not different between treated and control animals, though there was a transient hyperglycemia 1 h after treatment, and both treated groups became hypoglycemic after ten days. The results indicate that TCDD altered serum insulin levels which were not coupled to changes in serum glucose.     

Toxicological assessment of chlorinated diphenyl ethers in the rat

Chlorinated diphenyl ethers are environmental contaminants that have been found in Great Lakes fish and birds. Because of their presence in the food chain, and potential for human exposure, the present short-term study was conducted to assess their toxicity. Groups of 10 male and 10 female rats were each given by gavage 2,2',4,4'6-pentachlorodiphenyl ether (CDE1), 2,2',4,4',5,6-hexachlorodiphenyl ether (CDE2) or 2,2',3,3',4,6'-hexachlorodiphenyl ether (CDE3) at dose levels of 0.04, 0.4, 4.0 or 40 mg/kg b.w./day for a period of 28 days. The control group received an equivalent volume of corn oil only (0.5 ml/100 g b.w.). Treatment with the three CDE congeners did not result in suppression of growth rate or food consumption. Increased liver weights were seen in the animals of both sexes fed 40 mg/kg CDE2, in males treated with 40 mg/kg CDE1, and in females with 40 mg/kg CDE3. Hepatic microsomal aminopyrine demethylase activity was significantly higher in the male rats administered 40 mg/kg CDE2, and aniline hydroxylase activity was elevated in the females following the same treatment. Serum glucose, calcium, protein and urea nitrogen of CDE1-treated males were higher than the control. Levels of uric acid, potassium and LDH of CDE3-treated females were also elevated. No hematological changes were observed. Histological examination revealed that the liver and thyroid were the target organs affected by CDE treatment but the morphological changes were mild even at the highest dose level. Changes in the liver consisted of nuclear vesiculation and increased cytoplasmic volume. Alterations in the thyroid were characterized by increased epithelial height and follicular collapse. Based on the data presented above, the 3 CDE congeners can only be considered moderately toxic in the rat.     

Toxicological assessment of chlorinated diphenyl ethers in the rat

Abstract

Chlorinated diphenyl ethers are environmental contaminants that have been found in Great Lakes fish and birds. Because of their presence in the food chain, and potential for human exposure, the present short‐term study was conducted to assess their toxicity. Groups of 10 male and 10 female rats were each given by gavage 2,2’,4,4'6‐pentachlorodiphenyl ether (CDE1), 2,2’,4,4’,5,6‐hexachlorodiphenyl ether (CDE2) or 2,2’,3,3’,4,6'‐hexachlorodiphenyl ether (CDE3) at dose levels of 0.04, 0.4, 4.0 or 40 mg/kg b.w./day for a period of 28 days. The control group received an equivalent volume of corn oil only (0.5 ml/100 g b.w.). Treatment with the three CDE congeners did not result in suppression of growth rate or food consumption. Increased liver weights were seen in the animals of both sexes fed 40 mg/kg CDE2, in males treated with 40 mg/kg CDE1, and in females with 40 mg/kg CDE3. Hepatic microsomal aminopyrine demethylase activity was significantly higher in the male rats administered 40 mg/kg CDE2, and aniline hydroxylase activity was elevated in the females following the same treatment. Serum glucose, calcium, protein and urea nitrogen of CDE1‐treated males were higher than the control. Levels of uric acid, potassium and LDH of CDE3‐treated females were also elevated. No hematological changes were observed. Histological examination revealed that the liver and thyroid were the target organs affected by CDE treatment but the morphological changes were mild even at the highest dose level. Changes in the liver consisted of nuclear vesiculation and increased cytoplasmic volume. Alterations in the thyroid were characterized by increased epithelial height and follicular collapse. Based on the data presented above, the 3 CDE congeners can only be considered moderately toxic in the rat.     

Organochlorine concentrations in diseased vs. healthy gull chicks from the northern Baltic

The population decline of the nominate lesser black-backed gull Larus fuscus fuscus in the Gulf of Finland (northern Baltic) is caused by an exceedingly high chick mortality due to diseases. The chick diseases include degeneration in various internal organs (primarily liver), inflammations (mainly intestinal), and sepsis, the final cause of death. The hypothesis of starvation causing intestinal inflammations (leading to sepsis) was tested by attempting to reproduce lesions in apparently healthy herring gull L. argentatus chicks in captivity. The herring gull chicks were provided a similar low food-intake frequency as observed for the diseased chicks in the wild. However, empty alimentary tract per se did not induce the intestinal inflammations and therefore, inflammations seem to be innate or caused by other environmental factors in the diseased lesser black-backed chicks. They had very high concentrations of PCB in their liver; but the concentrations were not significantly higher than those of the healthy herring gull chicks, indicating a common exposure area for both species (i.e. the Baltic Sea). When compared to NOEL and LOEL values for TEQs in bird eggs our TEQ levels clearly exceed most or all of the values associated with effects. Compared with published data on fish-eating waterbirds, the DDE concentrations in the diseased lesser black-backed chicks were well above the levels previously correlated with decreased reproduction, while the residues in apparently healthy herring gulls were below those levels. The DDE/PCB ratio in lesser black-backs was significantly elevated, indicating an increased exposure to DDTs as compared with most other Baltic and circumpolar seabirds. The possible exposure areas of DDT in relation to differential migration habits of the two gull species are discussed.     

Changes in levels of essential elements in suckling rats exposed to zinc and mercury

The effect of mercury and its interaction with zinc on the content of essential metals in tissues from neonate rats was investigated. Three-day-old Wistar rats were treated with saline or 27 mg kg(-1)d(-1) ZnCl2 (s.c.) for five consecutive days. From the 8th to the 12th day of life, the rats received one daily dose of saline or 5.0 mg kg(-1) HgCl2 (s.c). Twenty-four hours after the last injection liver, kidneys and blood were collected for metal quantification. The HgCl(2) exposure induced alterations on metal levels, such as increase of Fe, Hg and Zn in liver, decrease of Fe and Mg and increase of Cu and Hg contents in kidneys. The Hg exposure also increased Hg levels in the blood. The treatment with ZnCl2, administered previously to HgCl2, partially prevented the increase of Fe in the liver, and not only prevented the decrease of renal Mg but also increased it to levels higher than those found in control group. The Zn-Hg rats also presented higher renal Cu levels, and showed partially lower blood and hepatic Hg levels and higher renal Hg levels. The pre-administration of Zn caused no severe alterations in levels of essential metals (Cu, Fe, Mg and Mn). In short, Zn appears to be an alternative treatment of Hg poisoning in young animals in comparison to chelating drugs since these have low metal selectivity.     

Chronic effects of mercuric chloride on the activities of some enzymes in certain tissues of the fresh water murrel,

Alterations in the activities of some enzymes in the brain, gills, intestine, kidney, liver and muscles have been examined in the fresh water murrel, , after exposure to a sublethal concentration of mercuric chloride (3 μg/1) for 15, 30 and 60 days. The results revealed that after 15 days of exposure amino acid oxidase activity was elevated in brain and liver and inhibited in intestine. The activity of xanthine oxidase was increased in gills, and inhibited in kidney. Thirty days exposure produced significant inhibition in the activities of malate dehydrogenase in liver, glutamate dehydrogenase in gills and brain, aminoacid oxidase in gills, and xanthine oxidase in liver and intestine. In contrast, glutamate dehydrogenase in intestine, kidney and liver and aminoacid oxidase in brain and liver were elevated. After 60 days of treatment, a decrease in the activity of glucose-6-phosphatase was recorded in gills, intestine, kidney and liver. Hexokinase activity in kidney and liver, and malate dehydrogenase in all the six tissues were inhibited. Glutamate dehydrogenase activity in intestine, kidney and liver remained higher than in control fish. In brain, kidney and liver the activity of aminoacid oxidase was elevated, but in gills the enzyme activity decreased. Xanthine oxidase activity was inhibited in intestine and liver.     

Chronic effects of mercuric chloride on the activities of some enzymes in certain tissues of the fresh water murrel, Channapunctatus

Alterations in the activities of some enzymes in the brain, gills, intestine, kidney, liver and muscles have been examined in the fresh water murrel, $\text{Channa}$$\text{punctatus}$, after exposure to a sublethal concentration of mercuric chloride (3 μg/1) for 15, 30 and 60 days. The results revealed that after 15 days of exposure amino acid oxidase activity was elevated in brain and liver and inhibited in intestine. The activity of xanthine oxidase was increased in gills, and inhibited in kidney. Thirty days exposure produced significant inhibition in the activities of malate dehydrogenase in liver, glutamate dehydrogenase in gills and brain, aminoacid oxidase in gills, and xanthine oxidase in liver and intestine. In contrast, glutamate dehydrogenase in intestine, kidney and liver and aminoacid oxidase in brain and liver were elevated. After 60 days of treatment, a decrease in the activity of glucose-6-phosphatase was recorded in gills, intestine, kidney and liver. Hexokinase activity in kidney and liver, and malate dehydrogenase in all the six tissues were inhibited. Glutamate dehydrogenase activity in intestine, kidney and liver remained higher than in control fish. In brain, kidney and liver the activity of aminoacid oxidase was elevated, but in gills the enzyme activity decreased. Xanthine oxidase activity was inhibited in intestine and liver.     

Thiram‐induced toxic liver injury in male sprague‐dawley rats

Abstract

A single i.p. dose (120 mg/kg) of thiram given to male Sprague‐Dawley rats caused a significant increase in the activity of SGOT and SGPT 24 hr post‐treatment indicating liver damage. A considerable diminution in the serum cholinesterase activity was also noted in the treated rats as against the control animals. Additional evidence for thiram‐induced liver toxicity is provided by the observation that there was approximately 50% inhibition of the activity of hepatic microsomal benzphetamine N‐demethylase with a concomitant decrease in the concentration of cytochrome P‐450, an important component of the mixed‐function oxidase system. Although not significant, hepatic glutathione levels were also depleted by thiram, probably making the liver susceptible to toxic injury.     

LIPID PEROXIDATION AND ANTIOXIDANT ENZYME ACTIVITY IN DIFFERENT ORGANS OF MICE EXPOSED TO LOW LEVEL OF MERCURY

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.     

Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (p<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.     

Residues of lindane and its metabolites in eggs, chicks, and body tissues of hen pheasants after ingestion of lindane-14C via treated wheat seed or gelatin capsules.

Studies were carried out to investigate possible contamination of pheasants with residues of lindane used as seed dressings for the control of wireworms in cereal crops. One group of laying hen pheasants was fed 20 mg of lindane-14C in gelatin capsules while another group was fed wheat seed treated with 100 ppm of lindane-14C for 15 days. Residues in eggs were monitored for about 70 days. Residues in chicks hatched from the eggs were also measured. Concentrations of residues in muscle, liver, brain, and fatty tissues were determined at various times. 14C-labeled residues in eggs increased sharply in the capsule treated group and reached an average maximum of about 19 ppm in 8 days. This level decreased to less than 0.5 ppm in about 50 days. Residues in eggs from the pheasants fed treated seed increased gradually to an average maximum of 17 ppm 22 days after commencement of the feeding program. This level decreased to less than 0.5 ppm 50 days later. Residues in hatched chicks were significantly lower than those in the eggs. Highest concentrations of residues were found in fatty tissues which decreased to non-detectable level in 6 months. Several chlorobenzene metabolites were identified in egg yolk and chick tissues. Chlorophenolic metabolites were indicated only in chicks.     

Thiram-induced toxic liver injury in male Sprague-Dawley rats

A single i.p. dose (120 mg/kg) of thiram given to male Sprague-Dawley rats caused a significant increase in the activity of SGOT and SGPT 24 hr post-treatment indicating liver damage. A considerable diminution in the serum cholinesterase activity was also noted in the treated rats as against the control animals. Additional evidence for thiram-induced liver toxicity is provided by the observation that there was approximately 50% inhibition of the activity of hepatic microsomal benzphetamine N-demethylase with a concomitant decrease in the concentration of cytochrome P-450, an important component of the mixed-function oxidase system. Although not significant, hepatic glutathione levels were also depleted by thiram, probably making the liver susceptible to toxic injury.     

Protective effects of seaweeds against liver injury caused by carbon tetrachloride in rats

Three species of seaweeds collected from Tung Ping Chau, Hong Kong, were screened for their hepatoprotective activity using carbon tetrachloride (CCl4)-induced liver injury in the rat as a model of chemical hepatitis. A single oral dose of 1.25 ml/kg of CCl4 was able to produce significantly elevated levels of serum glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transminase (GOT). Administration of 150, 300 and 600 mg/kg of aqueous extracts from Myagropsis myagroides, Sargassum henslowianum and S. siliquastrum, respectively, significantly reduced the CCl4-induced acute elevation in the levels of GPT and GOT in rats. The same result was also seen in the histopathological study of liver tissue. The seaweed crude extracts probably acted to protect against CCl4-induced liver injury through their antioxidant properties.     

Effects of sub-chronic low-level dietary intake of chlordane on rats with cirrhosis of the liver.

Male rats, 60 days old, were treated with chlordane during or after induction of liver cirrhosis with carbon tetrachloride to determine the effect of treatment with chlordane on the response of the rats to the disease. When liver cirrhosis was induced simultaneously with chlordane treatment the disease symptoms were aggravated; the lipid content of the tissue was lowered significantly, growth rate was significantly lower than controls and there was no apparent replacement of damaged liver tissue by liver growth. The cytochrome P450 content of the liver was similar after both treatments. Continuation of the chlordane treatment after termination of the carbon tetrachloride treatment brought about a more rapid recovery from the induced cirrhotic condition. All these responses were to a dose range one tenth the recommended "no effect" level for healthy animals.     

Temporal induction pattern of hepatic cytochrome P450 1A in thermally acclimated dab (Limanda limanda) treated with 3,3′,4,4′-Tetrachlorobiphenyl (CB77)

Mature male dab (Limanda limanda) acclimated at 10° and 16°C were orally administered a single dose of 0.5 mg/kg 3,3′,4,4′-tetrachlorobiphenyl (CB77). At both temperatures, levels of cytochrome P450 1A (CYP1A) protein and 7-ethoxyresorufin O-deethylase (EROD) activity showed a two to six fold induction 40 days after CB77 treatment compared to control groups. Maximum responses of both EROD activity and CYP1A protein for the warm-acclimated fish were observed at 5 days after treatment. For the cold-acclimated fish a slow, progressive elevation for both EROD activity and CYP1A protein was observed and maximum responses were measured 40 days after treatment. Absolute EROD activity and CYPIA protein levels of fish from both temperatures were equally high at 40 days after treatment. Since in the control groups EROD activity and CYP1A protein levels were higher in the cold-acclimated fish, the magnitude of induction was higher in the warm acclimated ones. The highest concentrations of CB77 in muscle of fish from both temperatures were found at 5 and 10 days after treatment. The liver somatic index (LSI) showed 1.5 fold significantly higher values for the fish acclimated at 10°C.     

Effects of sub‐chronic low‐level dietary intake of chlordane on rats with cirrhosis of the liver.

Abstract

Male rats, 60 days old, were treated with chlordane during or after induction of liver cirrhosis with carbon tetrachloride to determine the effect of treatment with chlordane on the response of the rats to the disease. When liver cirrhosis was induced simultaneously with chlordane treatment the disease symptoms were aggravated; the lipid content of the tissue was lowered significantly, growth rate was significantly lower than controls and there was no apparent replacement of damaged liver tissue by liver growth. The cytochrome P₄₅₀ content of the liver was similar after both treatments. Continuation of the chlordane treatment after termination of the carbon tetrachloride treatment brought about a more rapid recovery from the induced cirrhotic condition. All these responses were to a dose range one tenth the recommended “no effect”; level for healthy animals.     

Tissue distribution and effects on hepatic xenobiotic metabolising enzymes of 2,3,3',4,4'-pentachlorobiphenyl (PCB-105) in COD (Gadus morhua) and rainbow trout (Oncorhynchus mykiss)

2,3,3',4,4'-Pentachlorobiphenyl, PCB-105 (IUPAC no. 105) was orally administered twice with a 4-day interval between dosings (total dose 10 mg kg(-1) body weight) to gonadally immature cod and rainbow trout of both sexes. The fish were killed 9 and 17 days after the first treatment, and the effects of PCB-105 on hepatic xenobiotic metabolising enzymes were determined by examining the cytochrome-P450-dependent ethoxyresorufin-O-deethylase (EROD) and aldrin epoxidase activities, and the EROD-catalysing P450 1A1 protein by indirect enzyme-linked immunosorbent assay (ELISA). Glutathione S-transferase activity towards 1-chloro-2,4-dinitrobenzene was included. The hepatic levels of the compound were determined. In addition, the distribution patterns of radio-labelled PCB-105 were studied by whole-body autoradiography. In exposed rainbow trout EROD activity and P450 1A1 by enzyme linked immunosorbent assay (ELISA) were significant induced, while GST activity was significant reduced. Exposed cod did not show significantly different enzyme values from controls, but percentage fat in the liver was significantly reduced. The whole cod liver contained about 1000 times more PCB-105 than the corresponding trout liver, and on a fat-weight basis the PCB level was five to six times higher in cod liver than in the rainbow trout liver. The autoradiographical investigation revealed high concentrations of radiolabelled compound in the liver and the brain of cod, while in rainbow trout the radiolabel was mainly confined to extrahepatic fat depots. These results demonstrate that the mono-ortho chlorinated coplanar analogue, PCB-105, has a different distribution pattern in the two fish species and that the potential for induction of the hepatic xenobiotic metabolising enzyme system seems to be lower in the cod than in the rainbow trout.     

Inhalation toxicity studies of thimet (phorate) in male Swiss albino mouse, Mus musculus: I. Hepatotoxicity

Biochemical and histopathological changes in serum and liver of the male Swiss Albino mouse, Mus musculus, exposed subchronically to the recommended field dose of Thimet (6728.5 mg m(-3)) in a whole body inhalation chamber were studied in the second, fourth, sixth, eighth, tenth and twelfth week of exposure. A significant rise in Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT) activities were observed throughout the experiment. Alkaline phosphatase (ALP) activity showed a significant rise from the fourth week of exposure until the end of the experiment. The rise in the activities of these enzymes suggested hepatocellular necroinflammatory disease. Total bilirubin level was increased significantly throughout the experiment (indicative of jaundice); however the direct bilirubin level was significantly high in the tenth and twelfth week of exposure and indirect bilirubin showed a significant rise from the fourth week of exposure until the end of the experiment. Changes in bilirubin levels (direct and indirect) suggested both prehepatic and hepatocellular hyperbilirubinaemia. The biochemical changes observed and fatty change in the liver were confirmed by histopathological studies. Liver lesions were present throughout the experimental period. These consisted of mild to severe multifocal cloudy, hydropic and fatty degenerations, with necrosis. After a 30-day recovery period most of the histopathological and biochemical changes except the AST level were almost back to normal. These results suggest the inhalation of Thimet (Phorate) at the recommended field dose could affect the liver of Mus musculus.     

Alterations of lipid profile in plasma and liver of diabetic rats: effect of hypoglycemic herbs

The effect of three species of hypoglycemic herbs (Termis, Halfa barr, or Kammun Quaramany) on the lipid profile was investigated in plasma and liver tissues of diabetic and herbs-treated diabetic rats. This profile includes total lipids (TL), triglycerides (TG), cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL). A dose of 1.5 ml of aqueous suspension of each herb/100 g body weight (equivalent to 75 mg/100 g body weight) was orally administered daily to alloxan-diabetic rats for four weeks. The present study showed 2-fold increase (p<0.05) in the plasma glucose level of diabetic rats, which received alloxan as a single dose of 120 mg/kg body weight, relative to the mean value of control group. This elevated glucose level was restored to its normal level after treatment with any one of the three herbs. Furthermore, the levels of TL, TG, cholesterol, LDL and VLDL were significantly (p<0.05) increased in the plasma and the liver tissues of diabetic rats compared to the control group, whereas HDL level was significantly (p<0.05) decreased. The plasma levels of all above parameters were normalized after treatment of the diabetic rats with Kammun Quaramany. Treatment of diabetic rats with Tennis normalized TG, cholesterol, LDL and VLDL levels, but Halfa barr restored the induced levels of plasma cholesterol, LDL and HDL to their normal levels. On the other hand, treatment with any of the three herbal suspensions could not restore the concentrations of the all tested parameters in the liver. These data demonstrated that the glycemic control of any of the three herbal suspensions was associated with their hypocholesterolemic effects on the hypercholesterolemia of the alloxan-induced diabetic rats. Moreover, the Kammun Quaramany showed the most potent effect.