Effects of phosphorothionate on the reproductive system of male rats

Acute and Sub-acute toxic effects of a new pesticide phosphorothionate coded as RPR-V on testis of albino rat were studied. For the acute study, rats received a single dose of 30 mg/kg of RPR-V and sacrificed after 24 hours. For the Subacute study, 1.42 mg/kg/day was administered orally to rats for 10 days and 21 days. Acute exposure of rats to RPR-V brought no change either in the Gonadosomatic Index (GSI) or in the structure of testis or in the serum levels of Testosterone. Similarly, no significant change was observed in the Glutathione S-transferase (GST) activity. But, in testis there was significant increased in the reduced Glutathione (GSH) and Acid Phosphatase (AcP), whereas Alkaline Phosphatase (AkP) levels decreased significantly at 24hr post treatment. On 7th day (withdrawal period) after the cessation of the treatment the GSH, AcP, and AkP levels reached to near control. The sub-acute study revealed a significant post treatment. Due to RPR-V treatment the testis AcP levels increased significantly at 21st day of medication but AkP levels decreased both at 10th and 21st day of post treatment. Histopathological studies showed that after 10th day testis showed considerable loss of spermatozoids and at 21st day complete derangement of cellular organization was observed. Testosterone levels decreased significantly after 10th day and remained significantly low at 21st day. However, withdrawal studies showed a recovery in testis of rat treated with RPR-V. GST, GSH, GSI, AcP and AkP values were recovered, testosterone levels were also recovered but recovery in testis structure remained at a low profile.     

Studies on thallium toxicity, its tissue distribution and histopathological effects in rats

The distribution of thallium (Tl) in the body and its toxic effect on the histology and function of the liver and kidney of rats after Tl administration were investigated using biochemical and histopathological assays. Male albino rats exhibited a markedly dose-dependent increase in the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) at 16 h after an intraperitoneal injection of 30, 60 or 120 mg/kg Tl. The serum level of creatinine in the rats injected with 30 mg/kg Tl, elevated significantly after 4 days of administration. The distribution of Tl in the tissues of intoxicated rats was uneven. The content of Tl was found to be highest in the kidney, followed by ileum, stomach and liver. Histological examination demonstrated frequent occurrence of hepatocyte necrosis and vacuolation in the liver and pathological changes of renal tubules in the treated rats.     

Disposition of vanadium in rat tissues at different age

Tissue vanadium levels were determined in rats of different age by neutron activation analysis. The vanadium concentrations in the tissues of rats 21 days old are of the order of few tens of ng/g. Significant depletions of these concentrations were observed in kidney, liver lung and spleen at 115 days postnatal period. At this time the vanadium content in all tissues analysed did not exceed 10 ng/g.     

Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats

Recent studies have reported on the toxicity and related oxidative stress of selenium and mercury. The present study compares the effects of Se as sodium selenite (Na2SeO3) and Hg as mercuric chloride (HgCl2) separately and in combination. Rats received repeated oral doses of Se (0.5 micromol/ml), Hg (0.5 micromol/ml), or Se in combination with Hg (0.5 micromol/ml of each) for 5 consecutive days. Rat serum, brain and liver samples were collected for biochemical assays. The following biochemical alterations occurred in response to Hg treatment: protein content (brain and liver), acetylcholinesterase (AChE) (brain and serum), acid and alkaline (AcP and AlP) phosphatases (plasma and liver) and glutathione S-transferase (GST) (plasma and liver) activities were significantly (P<0.05) decreased, while lactate dehydrogenase (LDH) (plasma, brain and liver), aspartate and alanine aminotransferase (AST, ALT) (serum and liver) activities were significantly increased. Thiobarbituric acid reactive substances (TBARS) was significantly increased in brain and liver. Effect of Se alone included decreased AcP, AlP and GST (serum and liver) activities. However, LDH (serum, brain and liver) and AST (liver) and TBARS (brain and liver) increased. Selenium in combination with Hg partially or totally alleviated the toxic effects of Hg on different studied enzymes. It is concluded that Se could be able to antagonize the toxic effects of mercury.     

Regulatory effects of dioxin-like and non-dioxin-like PCBs and other AhR ligands on the antioxidant enzymes paraoxonase 1/2/3

Paraoxonase 1 (PON1), an antioxidant enzyme, is believed to play a critical role in many diseases, including cancer. PCBs are widespread environmental contaminants known to induce oxidative stress and cancer and to produce changes in gene expression of various pro-oxidant and antioxidant enzymes. Thus, it appeared of interest to explore whether PCBs may modulate the activity and/or gene expression of PON1 as well. In this study, we compared the effects of dioxin-like and non-dioxin-like PCBs and of various aryl hydrocarbon receptor (AhR) ligands on PON1 regulation and activity in male and female Sprague-Dawley rats. Our results demonstrate that (i) the non-dioxin-like PCB154, PCB155, and PCB184 significantly reduced liver and serum PON1 activities, but only in male rats; (ii) the non-dioxin-like PCB153, the most abundant PCB in many matrices, did not affect PON1 messenger RNA (mRNA) level in the liver but significantly decreased serum PON1 activity in male rats; (iii) PCB126, an AhR ligand and dioxin-like PCB, increased both PON1 activities and gene expression; and (iv) even though three tested AhR ligands induced CYP1A in several tissues to a similar extent, they displayed differential effects on the three PONs and AhR, i.e., PCB126 was an efficacious inducer of PON1, PON2, PON3, and AhR in the liver, while 3-methylcholantrene induced liver AhR and lung PON3, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent AhR agonist, increased only PON3 in the lung, at the doses and exposure times used in these studies. These results show that PCBs may have an effect on the antioxidant protection by paraoxonases in exposed populations and that regulation of gene expression through AhR is highly diverse.     

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.     

Subacute effects of a phosphorothionate pesticide on mixed function oxidases of Wistar rats

Subacute oral toxicity of a newly developed phosphorothionate insecticide (2-butenoic acid-3-(diethoxy-phosphinothioyl) methyl ester), coded as RPR-2, was studied in male rats by oral (multiple) intubation of low (0.014 mg kg(-1) day(-1)), medium (0.028 mg kg(-1) day(-1)), and high (0.042 mg kg(-1) day(-1)) dose for 90 days. The medium and high dose produced toxic symptoms along-with some mortality (20%) occurred in the high dose treated rats. The medium and high doses caused significant inhibition in cytochrome P-450 activity in liver, lung, kidney and brain tissues at 45 and 90 days. The high dose caused significant decrease in cyt.b5 activity of all the four tissues at 45 and 90 days. Whereas, medium dose brought such effect in liver and lung at 45 and 90 days. Kidney and brain cyt.b5 activity decreased significantly at 90th day due to medium dose. Low dose also caused inhibition in cyt.b5 activity in brain at 90th day. Cytochrome P-450 reductase activity was decreased significantly in liver,     

Subacute effects of a phosphorothionate pesticide on mixed function oxidases of wistar rats

Abstract

Subacute oral toxicity of a newly developed phosphorothionate insecticide (2‐butenoic acid‐3‐(diethoxy‐phosphinothioyl) methyl ester), coded as RPR‐2, was studied in male rats by oral (multiple) intubation of low (0.014 mg kg^‐1 day^‐1), medium (0.028 mg kg^‐1 day^‐1), and high (0.042 mg kg^‐1 day^‐1) dose for 90 days. The medium and high dose produced toxic symptoms along‐with some mortality (20%) occurred in the high dose treated rats. The medium and high doses caused significant inhibition in cytochrome P‐450 activity in liver, lung, kidney and brain tissues at 45 and 90 days. The high dose caused significant decrease in cyt.b₅ activity of all the four tissues at 45 and 90 days. Whereas, medium dose brought such effect in liver and lung at 45 and 90 days. Kidney and brain cyt.b₅ activity decreased significantly at 90^th day due to medium dose. Low dose also caused inhibition in cyt.b₅ activity in brain at 90^th day. Cytochrome P‐450 reductase activity was decreased significantly in liver, lung, kidney and brain at 45 and 90^th by the medium and high dose. The results indicated that RPR‐2 had potential to modulate hepatic and extra‐hepatic cyt.P‐450 dependent monooxygenase system of rat due to subacute exposure. These metabolic alterations were quite reversible after 28 days withdrawal of treatment.     

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.     

Reproduction study of toxaphene in the rat

The purpose of the present study was to investigate in rats the reproductive effects of toxaphene, an insecticidal mixture which has been identified as a pollutant in the Great Lakes ecosystem. Groups of 30 female and 15 male weanling rats were given toxaphene in the diets at 0, 4.0, 20, 100 or 500 ppm in a 1 generation 2 litter reproduction study. Toxaphene treatment at the levels studied had no effects on the litter size, pup weight, fertility, or gestation and survival indices. Toxic effects in the parental rats included depressed weight gain, elevated serum cholesterol, and increased liver and kidney weight and hepatic microsomal enzyme activities. Most of these effects were associated only with 500 ppm toxaphene treatment. Treatment-related histological changes in the liver, thyroid and kidney of adult rats were observed at levels as low as 20 ppm. Based on the data presented, the no observable adverse effect dose of toxaphene was considered to be 4.0 ppm in the diet (0.29-0.38 mg/kg b.w./day depending on the amount of dietary intake).     

Biochemical study on the protective role of folic acid in rabbits treated with chromium (VI)

Deleterious effects of chromium (VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. Therefore, the present study was carried out to determine the effectiveness of folic acid (FA) in alleviating the toxicity of chromium (VI) on certain biochemical parameters, lipid peroxidation, and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg FA and 0 mg Cr(VI)/kg BW (control); 8.3 microg FA/kg BW; 5 mg Cr(VI)/kg BW; 5 mg Cr(VI) plus 8.3 microg FA/kg BW, respectively. Rabbits were orally administered their respective doses every day for 10 weeks. Results obtained showed that Cr(VI) significantly (P < 0.05) increased the levels of free radicals and the activity of glutathione S-transferase (GST), and decreased the content of sulfhydryl groups (SH groups) in liver, testes, brain, kidney, and lung. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and lactate dehydrogenase (LDH) were significantly decreased in liver and testes due to Cr(VI) administration. Also, AlP and AcP activities were significantly decreased in kidney and lung. The activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Contrariwise, the activities of AST and ALT were significantly increased in plasma, while AlP and AcP decreased. Chromium (VI) treatment caused a significant decrease in plasma total protein (TP) and globulin, and increased total lipids (TL), cholesterol, glucose, urea, creatinine, and bilirubin concentrations. Folic acid alone significantly decreased the levels of free radicals in liver, brain, and kidney, and increased the content of SH-group. The activities of AST, ALT, and LDH in liver; AST, ALT, AlP, AcP, and LDH in testes; AcP in kidney; AlP and AcP in lung, and LDH in brain were significantly increased. Plasma TP and albumin were increased, while urea and creatinine were decreased. The presence of FA with Cr(VI) restored the changes in enzyme activities and biochemical parameters. In conclusion, folic acid could be effective in the protection of chromium-induced toxicity.     

Biochemical alterations in euryhaline fish, Oreochromis mossambicus exposed to sub-lethal concentrations of an organophosphorus insecticide, monocrotophos

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (1.15 mg l(-1)) of a organophosphorus insecticide, monocrotophos (MCP) for 30 days and allowed to recover for seven days. Alanine aminotransferase (ALAT), aspartate aminotransferase (AAT), acid phosphatase (AcP), alkaline phosphatase (ALP), glycogen, lactate dehydrogenase (LDH), Reduced glutathione (GSH), gluthathione-S-transferase (GST) and acetylcholinesterase (AChE), were assayed in plasma and different tissues at regular intervals of day -3, -7, -15, -30 and after recovery period of seven days. The ALAT and AAT activities were increased in plasma and kidney, where as liver and gill showed decrease. Increase in AcP and ALP activities were observed in plasma, gill and kidney, and reduction of 42% and 50% was observed in liver. Glycogen was depleted in plasma, liver and gill indicates of typical stress related response of the fish with pesticide. LDH activity was decreased in liver and muscle, indicating tissue damage and muscular harm, but a significant increase in LDH activity in gill and brain was observed. Depletion in GSH activity was observed in all the tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic GST levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters studied in plasma and different tissues, after seven days recovery period. These results revealed that MCP affects the intermediary metabolism of O. mossambicus and that the assayed enzymes can work as good biomarkers of organophosphorus contamination.     

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.     

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.     

Toxicity of trichlorotoluene isomers: a 28-day feeding study in the rat

Groups of 10 male and 10 female rats were fed alpha,alpha,alpha-, alpha,2,6- or 2,3,6- trichlorotoluene (TCT) in their diet at 0, 0.5, 5.0, 50 or 500 ppm for 28 days. Growth rate and food consumption were not affected by treatment. No deaths occurred. Significant increases in liver weights were observed in male rats fed 5.0 and 500 ppm 2,3,6-TCT. Mild serum biochemical changes occurred in male rats. These included increased SDH activities in the groups fed 5.0 and 50 ppm alpha, alpha, alpha-TCT, and 5.0 ppm 2,3,6-TCT. Alpha, alpha, alpha-TCT at 500 ppm caused elevated LDH activities in male rats. Hepatic microsomal aminopyrine N-demethylase activities were increased in male rats fed 500 ppm alpha,2,6-TCT. Hematological parameters were not affected by treatment. Mild histological changes were seen in the liver, kidney and thyroid of treated rats. Data presented here suggest that alpha, alpha, alpha-, alpha,2,6- and 2,3,6-TCT possess a low order of oral toxicity in the rat.     

Biochemical stress response in freshwater fish Channa punctatus induced by aqueous extracts of Euphorbia tirucalli plant

Piscicidal activities of aqueous extracts of Euphorbia tirucalli were very well established, but their ultimate mode of action on fish metabolism was not yet known. Exposure of fishes over 24h or 96h to sub-lethal doses (40% and 80% of LC(50)) of aqueous extract of E. tirucalli stem-bark and latex, significantly (P<0.05) altered the level of total protein, total free amino acids, nucleic acids, glycogen, pyruvate, lactate and activity of protease, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase and cytochrome oxidase enzyme in liver and muscle tissues of freshwater fish Channa punctatus. The alterations in all these biochemical parameters were significantly (P<0.05) time- and dose-dependent. After 7d of withdrawal of treatment of 80% of LC(50) of E. tirucalli extracts shows that there was a partial recovery in the levels of glycogen but nearly complete recovery in total protein, total free amino acids, pyruvate, lactate, nucleic acids level and activity of protease, aspartate aminotransferase, alanine aminotransferase, acetylcholinesterase and cytochrome oxidase enzyme in both the tissues of fish. Thus aqueous extracts of E. tirucalli adversely affect respiratory pathway of fish and cause energy crisis during stress by suppressing ATP production. The reversibility of the action of the aqueous extracts would be an additional advantage in their use.     

Antioxidant response versus selenium accumulation in the liver and kidney of the Siberian sturgeon (Acipenser baeri)

The aim of this study was to examine the effects of selenium on concentrations of metabolites and enzyme activities acting as antioxidant markers in liver and kidney of Siberian sturgeon Acipenser baeri. Sturgeons were fed selenium cysteine for 30 and 60 d at 1.25, 5, 20 mg Se kg⁻¹. Selenium level in the control feed was 0.32 mg kg⁻¹. Se concentration was measured in liver, kidney and muscle of every specimen. Sturgeon accumulated Se in tissues with a clear dose-response relationship and the highest Se concentration was recorded in liver. This outcome is lined up with the findings obtained on the antioxidant markers evaluated in both tissues, and in which a dose-response for several biomarkers was recorded in liver. The superoxide dismutase activity in Se-treated fish was generally induced, while catalase activity was lower in liver or unaltered in kidney. The concentrations of glutathione S-transferase, glutathione reductase and total glutathione responded differently for both tissues and were induced in a different way at both endpoints. No changes of glyoxalase I activity were noted for both Se-treated tissues, while for glyoxalase II enzyme in liver a dose-related pattern was found showing a reversible effect (decreased and increased counteractive response) only in the 5 mg kg⁻¹ group. Moreover, the highest Se concentrations did not cause marked changes in malondialdehyde levels of liver and kidney. The enhancement of glutathione peroxidase activity in Se-treated sturgeon might have prevented the lipid peroxidation in both tissues, providing to the Siberian sturgeon a great defense ability versus the prooxidant effect of selenium.     

Impact of heavy metal pollution on the hemogram and serum biochemistry of the Libyan jird, Meriones libycus

The stress profiles of the hemogram and serum biochemistry were determined in the context of heavy metal (Cd, Cu, Hg, Ni and Pb) exposure in the wild libyan jird, Meriones libycus, from one of Riyadh’s polluted areas versus a reference site. Coupling the pronounced drop in platelets (PLT) (28%) and mean platelet volume (MPV) (17%) with the insignificant responses of other red blood cell indices, suggests bone marrow suppression that is characterized by thrombocytopenia as an initial abnormality. The species-specific stress leukogram for M. libycus is expressed by leukocytosis (66%), monocytosis (40%), lymphocytosis (23%) with eosinopenia (81%) and neutropenia (42%). Hyperglycemia (50%), hyper-low-density-lipoproteinemia (38%), hypocortisolism (85%) and hypotriglyceridemia (55%) depicted serum biochemistry profile. In polluted jirds, the elevated activities of pseudocholinesterase (PChE) and serum marker enzymes (alanine aminotransferase ALT, aspartate aminotransferase AST and creatine kinase CK) strongly suggest functional damage of the liver and/or heart. A potential role of PChE in low-density lipoprotein (LDL) metabolism is implied in the joint rise of both indices and in the recognized relationship between PChE and lipid metabolites. While increased utilization in lipid metabolism and energy synthesis could rationalize the inhibition of the normal patterns of triglycerides and lactate dehydrogenase (LDH), the inhibited activities of LDH could additionally be attributed to its hormetic behavior towards low and high metal concentrations. The overall findings presented here documented the relevance of M. libycus in biomonitoring and predicting the risk imposed on human populations living in polluted areas.