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Of the three dinitrobenzene isomers listed in Table 4-37 virus 2 discount nifostin 500mg with mastercard, only 1 virus 7th grade science discount nifostin 250 mg on line,3-dinitrobenzene virus 1980 cheap nifostin generic, not 1 antibiotics and period order nifostin from india,2-dinitrobenzene or 1,4-dinitrobenzene, is a potent testicular toxicant that targets the Sertoli cell. Similarly, the cerebellar neurotoxicity ascribed to 1,3-dinitrobenzene and 1,3,5-trinitrobenzene is not observed in animals dosed with 1,4-dinitrobenzene (Chandra et al. For example, 17 of 200 high-dose mice died during the period of exposure, and others displayed typical signs of toxicologically stressed animals, such as ataxia, lethargy, and circling. Eight distinct investigations of the immunotoxicological effects of nitrobenzene were carried out among the exposed mice, while some nonimmunotoxicological parameters were monitored in all animals. Examination of the mice at autopsy 24 hours after the final exposure showed hepatomegaly and splenomegaly in the mid- and high-dose groups, although the overall liver changes were slight. The affected spleens were dark red in color, with mild congestion in the red pulp areas and the appearance of occasional nucleated erythrocytes. Hemosiderin pigment was noted in the red pulp areas, a response thought to be indicative of erythrocyte dysfunction. Compound-related changes in organ weights were noted, including dose-dependent increases in the absolute and relative weights of liver, spleen, and kidney. A number of apparently compound-related effects in hematologic responses to nitrobenzene were observed, consistent with the concept of the erythrocyte as a primary target organ of nitrobenzene toxicity. Although no treatment-related differences in leukocyte differentials were observed after 14 days, there were striking changes in the percentage of circulating reticulocytes as a result of treatment (4. Other dose-dependent effects of nitrobenzene on clinical chemistry parameters included apparent increases in the levels of bilirubin and albumin but decreases in glucose concentration. In light of the changes observed in the spleen and hematologic parameters, Burns et al. Progenitor cells were 81 measured by incubating bone marrow cells with 10% colony stimulating factors isolated from either mouse fibroblast L-929 cells or mouse lung-conditioned medium. The number of nucleated cells/femur was increased dose dependently to a level of 62% above controls, with statistical significance seen in the low-dose group. As described by the authors, the number of colony-forming unit (granulocyte-monocyte) stem cells was the same as in controls when calculated per 105 bone marrow cells. However, the number of cells/femur and the number of colony-forming unit (granulocyte-monocyte) stem cells/femur were increased twofold in association with nitrobenzene treatment (Burns et al. Although there was a dose-dependent increase in spleen weight and spleen cell number 4 days after exposure to nitrobenzene, there was no difference in the splenic IgG responses to sheep erythrocytes as a result of nitrobenzene exposure. By contrast, nitrobenzene exposure caused a dose-dependent decrease in the IgM response to sheep erythrocytes on day 4 (40 and 34% for the mid- and high-dose nitrobenzene groups, respectively). According to the authors, this suppression could be accounted for by the observed compound-induced splenomegaly (Burns et al. However, treated mice recovered their ability to mount an IgM response within 20 days. Cells were isolated from excised spleen tissue after 15 days of nitrobenzene exposure and cultured for 3 days in the presence of four concentrations of the above mitogens. The amount of [3H]-thymidine incorporated into the cells over the last 18 hours of the incubation was taken as a measure of spleen cell proliferation. Similarly, in another sequence of observations, there were no differences in serum complement levels between nitrobenzene-exposed and control groups. However, this effect was considered to be a consequence of liver enlargement in nitrobenzenereceiving groups. Nitrobenzene exposure caused a dose-dependent decrease in lytic activity at all effector:target cell ratios tested. The same research report describes a series of experiments to evaluate the effect of nitrobenzene on host resistance to infection with Plasmodium berghei, Listeria monocytogenes, Streptococcus pneumoniae, herpes simplex type 2 virus, and the metastatic pulmonary tumor, B16F10. Similar differences were observed for different titers in mice exposed to 100 mg/kg nitrobenzene. Nitrobenzene exposure did not impair host resistance to herpes simplex virus, as measured by percent mortality or time to death. Nitrobenzene somewhat impaired host resistance at the highest level, indicating a modest depression of T-cell immunity. These results were thought to indicate that the 83 principal target of nitrobenzene toxicity was bone marrow, with consequent hematologic and immunotoxicological impacts. Cell counts from animals primed with aniline and challenged with either aniline or nitrosobenzene were consistent with controls. Similarly, the cell counts from animals primed with nitrosobenzene and subsequently challenged with aniline were not statistically significantly different from controls. In contrast, when animals were primed with nitrosobenzene and also challenged with nitrosobenzene, a statistically significant increase in cellularity was observed compared with controls. Neurotoxicity Studies Signs and symptoms of neurotoxicity following exposure to nitrobenzene have been reported as early as the 1900s. No epidemiological studies have been conducted on occupationally exposed cohorts; however, numerous case reports indicate neurological involvement following accidental or intentional exposure to nitrobenzene. Similarly, Stifel (1919) reported 16 cases of nitrobenzene poisoning from shoe dye. Many of the patients complained of headache, nausea, dizziness, and general malaise. In a more comprehensive report, Ikeda and Kita (1964) presented findings from a woman who was occupationally exposed to nitrobenzene. After about 6 weeks of working under these conditions, the woman presented with severe headache, nausea, vertigo, and numbness in her legs.
The frequency of positive titers gradually increases in the female population with aging antibiotic xtreme cheap nifostin 250mg mastercard. Even a low titer of antithyroid antibodies correlates with a degree of thyroid involvement by an autoimmune process antibiotics for uti in humans proven 500mg nifostin. The absence of antibodies has been documented in diagnosed cases of autoimmune thyroiditis antibiotic with birth control pills buy nifostin 100 mg otc, which may be explained by special characteristics of the antibody antibiotics for dogs and humans buy nifostin 500mg with amex, or because it forms complexes with thyroglobulins in the circulation and escapes detection. The presence of these circulating complexes has been documented in patients with thyroid autoimmune disorders. The thyroid membrane receptors are a group of immunoglobulin G (IgG) antibodies that interact with receptors on thyroid membranes. At present, classification of these IgG antibodies is operational, based on their method of detection. Antibodies to T4 and T3 have been found in several patients, most of whom had evidence of a thyroid autoimmune process such as goiter or hypothyroidism. In these cases, the underlying autoimmune process is most likely responsible for the hypothyroidism rather than hormone binding by the circulating antithyronine antibodies. Diagnostic Evaluation Fine-needle aspiration biopsy of the thyroid is useful in conjunction with clinical evaluation and serologic studies for the diagnosis of lymphocytic thyroiditis. Histologic examination of thyroid tissue demonstrates variable infiltration of the entire gland with lymphocytes. Germinal lymphoid centers are characteristic and destruction and distortion of normal thyroid follicles are apparent. The thyroid cells remain intact but are hypertrophied, although the usual heterogeneity of small, enlarged thyroid follicles, some containing flat epithelium, can also be seen. In advanced cases, there is almost complete destruction of normal thyroid tissue, with replacement by lymphocytes or fibrous tissue. Antithyroglobulin and/or antithyroid microsomal antibodies are found in moderate to high titers in more than 50% of patients, but the presence of antimicrosomal antibodies is considered to be more diagnostic. They are also complement-fixing antibodies that can induce cytotoxic changes in cells and consequently cause thyroid dysfunction. This disease is most likely if a patient has signs and symptoms of hyperthyroidism. The only definitively identified environmental factor causing T1D is congenital rubella infection. Reports of an association between diabetes and infection with coxsackievirus B and several other viruses have suggested other triggers for the disease. Most patients develop T1D in childhood or early adolescence, but it may occur at any age. Approximately 95% of patients who develop clinical diabetes before age 30 years have T1D. The central clinical feature is the requirement for exogenous insulin to maintain euglycemia. Autoantibodies to isletrelated antigens precede the development of clinical T1D by a prolonged period, often several years. An immunoglobulin in the sera of patients with insulinresistant diabetes appears to bind to a tissue receptor for insulin, which prevents some of the biological effects of insulin. In addition, antibodies that bind to and possibly kill pancreatic islet cells have been found in most young patients with T1D. A small subgroup of patients with T1D has demonstrated antireceptor antibody (InR), an IgG class of antibodies directed against the insulin receptor. Antibodies to InR may be directed to the binding site or to determinants away from the binding site for insulin. This type of chronic pancreatitis is characterized by an autoimmune inflammatory process in which prominent lymphocyte infiltration with associated fibrosis of the pancreas causes organ dysfunction. Although the cause of the disorder is unknown, it is thought to be a systemic autoimmune disorder. Autoimmune pancreatitis is rare, but an increasing number of cases has been reported since 2000. Although this condition can occur in both genders, it is at least twice as common in men as women. Various findings on imaging radiography are correlated with serologic and histologic analyses. It is important to diagnose autoimmune pancreatitis correctly on the basis of imaging, histology, and serology because it can mimic pancreatic cancer. Although a great potential exists for morbidity, it has a relatively low incidence. These antibodies generally bind to components in the adrenal cortex but affect only individual zones. Antibodies are generally low in titer and are not a direct reflection of adrenal cell damage. In women with premature ovarian failure, autoimmune destruction of the ovarian stroma has been observed. The disorder is distinguished by a mononuclear infiltrate of the pituitary gland and hypophysis.
Corticosteroids in acute traumatic brain injury: systematic review of randomised controlled trials antibiotics sinus infection npr buy nifostin mastercard. A multicenter trial on the efficacy of using tirilazad mesylate in cases of head injury antimicrobial resistance global report on surveillance buy discount nifostin line. What is the optimal method of administering these calories (enterally/parenterally/both) What should the composition of such support include with regard to carbohydrates antibiotic 875125 cheap generic nifostin canada, proteins antibiotic resistance reversal generic 100mg nifostin overnight delivery, and lipids What is the role of insulin in controlling serum glucose concentrations in this vulnerable patient population Changes from Prior Edition Additional evidence was identified and incorporated into revised recommendations that emphasize early nutrition and address the method of feeding. For glycemic control, the available evidence was inconsistent and insufficient to support a recommendation. The evidence for vitamins and supplements was insufficient, as only one small Class 2 study was identified in addition to the two Class 3 studies from the 3rd Edition, and these studied different vitamins and supplements. Applicability the studies of nutrition were predominately single-site studies, but they were conducted in a variety of locations. One multi-center study was conducted in the United States,8 while two of the single-site studies were conducted in the United States,10,16 and one each in Greece,7 the United Kingdom,11 France,9 Spain,12 Italy,13 China,15 and Brazil. Of the remaining 10, seven were rated Class 27-9,12-15 and are included with the three Class 2 studies from the 3rd Edition. Class 2 Studies the evidence from the Class 2 studies of nutrition is summarized in Table 8-2. There were 8 deaths in the enteral nutrition group and none in the parenteral nutrition group in the first 18 days, p<0. Class 2 Nutritional support within 5 days was associated with a significant reduction in 2-week mortality. Accelerated feeding met goals faster in the first week and there were fewer infections. Comparison of intensive (received continuous insulin infusion to maintain glucose levels between 4. Neurologic outcomes were not significantly different 90 in two studies13,14 while one study15 found some improvement in function at 6 months. For this reason, the evidence was rated as insufficient and no recommendation about glucose control can be made at this time. Therefore, there is insufficient evidence about the influence of vitamins and supplements to inform recommendations. Class 3 Studies the evidence from the Class 3 studies of nutrition is summarized in Table 8-3. Rapid correction of serum magnesium levels does not reverse the prognostic value of these markers. Continuous group reached 75% goals earlier, trend towards less infection in continuous feeding. Data Class Class 3 Results Conclusion Nasojejunal feeding permitted increased caloric intake and improved nitrogen balance. Infections, lymphocyte counts, albumin levels were the same in both groups as was outcome. One, new to this edition, reported that earlier feeding was associated with better outcomes at 3 months, although there was no significant difference at 6 months. Glycemic Control Glycemic control was the subject of two Class 3 studies from the 3rd Edition. Given this overlap and the fact that our evidence synthesis and these reviews reached similar conclusions, we decided to describe the systematic reviews here in the text rather than include their results in the evidence table. They identified 11 trials: seven are included in our review above; two were excluded for sample sizes under our requirement; and two did not include any of our required clinical or intermediate outcomes. The review authors concluded, as we did, that early feeding is associated with better outcomes. Additionally, the review authors pooled the trial results in order to compare parenteral to enteral routes and found no significant difference, with a slight trend toward better outcomes with parenteral nutrition. Nine of these are included in our review: one is pediatric only and is in the pediatric guideline; three had mixed ages, pathologies, or severity; and three had small sample sizes. Combining the studies to include those we excluded for sample size did 95 not lead to a different conclusion. This review also found that early feeding was associated with better outcomes, and that parenteral nutrition is associated with slightly better outcomes than enteral routes, but the difference is not significant. Energy expenditure in patients with severe head injury: controlled normothermia with sedation and neuromuscular blockade. Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury. Effect of early compared with delayed enteral nutrition on endocrine function in patients with traumatic brain injury: an open-labeled randomized trial. The favorable effect of early parenteral feeding on survival in head-injured patients. Prospective, randomized, controlled trial to determine the effect of early enhanced enteral nutrition on clinical outcome in mechanically ventilated patients suffering head injury. Gastric versus transpyloric feeding in severe traumatic brain injury: a prospective, randomized trial. Intensive insulin therapy after severe traumatic brain injury: a randomized clinical trial. Zinc supplementation is associated with improved neurologic recovery rate and visceral protein levels of patients with severe closed head injury.
Humans are facultative nose breathers virus 32 removal purchase online nifostin, while rodents are obligatory nose breathers infection leg pain buy genuine nifostin online. Olfactory degeneration observed following long-term nitrobenzene inhalation in rodents may zombie infection nokia 5228 purchase cheap nifostin line, therefore antibiotic yeast infection prevention purchase nifostin in united states online, not be relevant for humans, but supportive or refuting evidence is not available. However, bronchiolization of the alveoli is of relevance to both facultative and obligatory nose breathers. It has been proposed that metabolism of nitrobenzene involves the formation of reactive oxygen species (Han et al. The male reproductive toxicity of nitrobenzene affects the Sertoli cells (Allenby et al. The action of reactive oxygen species cannot be excluded as a causative factor here. Characterization of the Human Carcinogenic Potential Under the Guidelines for Carcinogen Risk Assessment (U. There are no nitrobenzene exposure data or studies in humans from which to assess a potential mechanism of action for cancer. Nitrobenzene caused neoplasia in a 2-year chronic inhalation study (Cattley et al. Although the probable human carcinogen, aniline, is a metabolite of nitrobenzene, there is no evidence that it is a causative agent (U. This is reflected in the use of a linear approach as a default option in extrapolating the carcinogenic potential of nitrobenzene. However, they were of short duration, used nontoxic doses, and only examined clinical signs. All dose-response assessments are therefore based on animal data obtained from chronic or subchronic studies. The study reported an abundance of toxic endpoints, including changes in absolute and relative organ weights, changes in hematologic parameters, and histopathologic outcomes. Methemoglobinemia, splenic congestion, and reticulocyte count in male F344 rats were considered as potential critical effects. The critical effect on which the RfD is based is well supported by several other oral gavage studies over time periods of up to 70 days (Kawashima et al. Nitrobenzene also displayed toxicity in reproductive and immunological studies but at doses higher than those used in the principal study. Inhalation RfC A few studies with nitrobenzene in human research subjects have been conducted that were of short duration with nontoxic doses, and their target was not pathological evaluation. There are four animal studies available dealing with inhalation toxicity of nitrobenzene, ranging in duration from acute to chronic. This study identified a variety of hematologic endpoints, above all methemoglobinemia, with several other outcomes secondary to hemolytic anemia. Rats were exposed to 0, 1, 5, and 25 ppm nitrobenzene and mice to 0, 5, 25, and 50 ppm nitrobenzene for 6 hours/day, 140 5 days/week (except holidays). This study identified a range of noncancer endpoints, of which bronchiolization of the alveoli was the most sensitive endpoint in both male and female mice. Olfactory degeneration was a sensitive endpoint in female mice and to a lesser extent in male mice. Bronchiolization of the alveoli and olfactory degeneration were chosen as co-critical effects for deriving the RfC, over methemoglobinemia, because of the greater extent and increasing severity of both endpoints with increasing concentration compared to the lack of a clear concentration-dependent response for methemoglobinemia at final sacrifice. The effects selected for RfC derivation, bronchiolization of the alveoli and olfactory degeneration in male and female B6C3F1 mice in the chronic study, were considered portal-of entry effects. Confidence in the principal study is high because it was a 2-year bioassay with a sufficient number of animals, and it is reasonable to assume that the endpoint is relevant to humans. Confidence in the database is rated high due to the existence of a 2-year inhalation study, a two-generation reproductive and developmental toxicity study, and a subchronic inhalation study. Oral Cancer Risk the lack of available data precludes an assessment of a potential cancer risk for humans following oral exposure to nitrobenzene. Inhalation Cancer Risk the mode of carcinogenic action of nitrobenzene remains poorly understood but, based on available studies, is not likely due to mutagenicity. Nitrobenzene was inactive in all bacterial mutagenicity assays and gave equivocal results in both in vivo and in vitro mammalian assay systems. Nitrobenzene caused tumors in multiple organs in both sexes in two species (rat and mouse) and in two different strains of rats in a 2-year inhalation study (Cattley et al. Nitrobenzene increased the incidence of lung adenomas and carcinomas in male B6C3F1 mice only, providing minimal evidence for point-of-entry carcinogenesis. Male F344 rats appeared to be the most sensitive animal and presented with tumors of the liver, kidney, and thyroid. Determination of partition and distribution coefficients with brush border membrane vesicles. Methylene blueabsorption, metabolism, and excretion in man and dog after oral administration. A case of acute nitrobenzene and aniline poisoning treated by exchange transfusion. The metabolism of nitrobenzene in the rabbit; o-, m- and p-nitrophenols, o-, m- and p-aminophenols and 4-nitrocatechol as metabolites of nitrobenzene. Absorption of nitrobenzene vapour through lungs and excretion of p-nitrophenol in urine. Detection of superoxide formation during aerobic microsomal reduction of nitro-compounds.
In the liver antibiotics for uti cause constipation buy nifostin discount, male mice presented with exposuredependent changes in centrilobular hepatocytomegaly and multinucleated hepatocytes antibiotics names order nifostin from india, up to 89 and 88% antibiotics resistant bacteria generic nifostin 250mg amex, respectively infection of the spine cheap 500 mg nifostin overnight delivery. In contrast, centrilobular hepatocytomegaly was undetectable in female mice, except for the highest dose (11% above controls), as were multinucleated hepatocytes (3% above controls). Selected noncancer histopathologic changes in B6C3F1 mice as a result of exposure to nitrobenzene via inhalation for 2 years Exposure concentration (ppm) Males Target tissue Liver Centrilobular hepatocytomegaly Multinucleated hepatocytes Lung Hyperplasia Bronchiolization Thyroid Follicular cell hyperplasia Nose Pigmented olfactory epithelium Degenerated olfactory epithelium a Females 25 44/65a 45/65a 8/65a 58/65a 7/65a 46/65a 32/65a 50 57/64a 56/64a 13/66a 62/66a 12/64a 49/66a 41/66a 0 0/51 0/51 0/53 0/53 2/49 0/52 0/52 5 0/61 0/61 2/60 55/60a 1/59 6/60a 19/60a 25 0/64 0/64 5/64a 63/64a 1/61 37/63a 47/63a 50 7/62a 2/62a 1/62 62/62a 8/61 29/61a 42/61a 0 1/68 2/68 1/68 0/68 1/65 0/67 1/67 5 15/65 14/65 2/67 58/67a 4/65 7/66 1/66 Statistically significantly different from control values, as calculated by the authors. The authors treated F344 rats and B6C3F1 mice (10 animals/sex/group) with 50, 100, 200, 400, and 800 mg/kg-day nitrobenzene in acetone, the responses being compared with those in animals painted with acetone alone. At 800 mg/kg-day, all rats and 9/10 male and 8/10 female mice died before the end of the experiment. Furthermore, surviving animals in the other exposure groups (dose levels not stated) displayed profound clinical signs of acute toxicity, including ataxia, dyspnea, circling, lethargy, and insensitivity to pain. Among the histopathologic findings, there was a marked degeneration of the testes in the males of both species and all nitrobenzene-receiving rats displayed congestion of the spleen. The incidence of congestion of the lungs was dose-dependently increased in males and females of both species. Vacuolization of the brain or brain stem was another characteristic histopathologic finding, the effects becoming apparent in rats exposed to nitrobenzene at 100 mg/kg or higher, in male mice exposed to 800 mg/kg, and in female mice exposed to 400 and 800 mg/kg nitrobenzene. Dose (mg/kg-day) 100 200 3/10 10/10 10/10 0/10 0/10 0/10 0/10 5/10 10/10 8/10 1/10 10/10 1/10 9/10 10/10 1/10 0/10 0/10 0/10 2/10 10/10 4/10 4/10 8/10 0 1/10 8/10 0/10 0/10 0/10 0/10 0/10 0/10 0/10 0/10 0/10 0/10 50 1/10 10/10 10/10 0/10 0/10 0/10 0/10 1/10 0/10 0/10 1/10 0/10 400 6/10 10/10 10/10 9/10 0/10 4/10 0/10 1/10 4/10 7/10 7/10 4/10 800 9/10 10/10 10/10 10/10 4/10 4/10 6/10 2/10 3/10 6/10 6/10 3/10 58 Table 4-26. This permitted spermatogenesis to be continually monitored during and after exposure to nitrobenzene. Six rats/group were subjected to this surgical procedure and, after a recovery period of 6 weeks, gavaged with a single dose of 300 mg/kg nitrobenzene in corn oil. Animals were housed in metabolic cages and assessed for the release of sperm to the urine for up to 100 days. Two other groups of rats, 45 exposed and 30 controls, were gavaged in a manner similar to the surgically altered subjects. These were serially sacrificed for histopathologic examination at various time points, up to 100 days. Output of sperm held steady after nitrobenzene administration for about 20 days then dropped to zero within 12 days and persisted at this level until day 48. Fifty days after treatment, sperm began to reappear in the urine of treated animals, ultimately achieving about 78% of control levels. Histopathologically, treated animals displayed degeneration of the seminiferous epithelium within 3 days of treatment, an effect characterized by the appearance of pachytene-derived giant cells and loss of the more mature elements of the seminiferous epithelium. Clear histopathologic signs of regeneration were apparent at about 21 days after treatment. However, at least some signs of the abnormal cellular architecture and tubular organization described above always remained. For example, approximately 10% of the tubules examined showed little evidence of spermatogenesis even at 8 weeks posttreatment, with mature spermatids rarely apparent. The authors interpreted their results in accordance with the known processes and time frame by which spermatogenesis occurs in F344 rats and presented a nomogram that correlated the spermatogenic cycle of the rats with the proposed chronology of nitrobenzene-induced lesions. Three rats at each dosage were sacrificed 2 and 5 days following nitrobenzene administration. Samples of blood were obtained by cardiac puncture to measure metHb, and 25 tissues and organs were excised for histopathologic examination. The liver, testes, and brain from all animals in the study were examined histopathologically, whereas histologic sections of other tissues were examined only in the high-dose and control groups. Hepatic centrilobular necrosis appeared inconsistently in rats given various doses of nitrobenzene, while hepatocellular nucleolar enlargement was consistently detected in rats given doses of nitrobenzene as low as 110 mg/kg. Lesions occurred in the seminiferous tubules of the testicles, with marked necrosis of primary and secondary spermatocytes following a single oral dose of 300 mg/kg (Bond et al. Furthermore, within 3 days of nitrobenzene administration, multinucleated giant cells were observed, and 61 decreased numbers of spermatozoa were observed in the epididymis. Histopathologic analyses indicated that nitrobenzene had no apparent effects on spermatogonia or the epididymal epithelium. In parallel to the observed histopathologic lesions in liver and testes, methemoglobinemia was increased to 25% immediately after dosing at 300 mg/kg, with a subsequent slow decline over the next 10 days. In a control experiment, the administration of sodium nitrite also induced methemoglobinemia but had no histopathologic effects on the testes and liver, suggesting that the histopathologic effects of nitrobenzene occurred through a direct action of the compound or its metabolites at the tissue site rather than as a secondary effect of metHb formation. Two further studies confirmed the association between orally administered nitrobenzene and the onset of toxic effects in the testes and epididymides. Parameters evaluated included the weights and histopathology of the testes and epididymides, together with an analysis of the count, motility, viability, and morphology of the sperm. Nitrobenzene at the high dose (60 mg/kg) induced a relative decrease in the weight of the epididymis, decreases in sperm motility and viability, and an increase in the incidence of morphologically abnormal sperm. Degeneration and decreases in spermatids and pachytene spermatocytes were specified as primary effects of nitrobenzene at this dose level. All subjects were examined for changes in testis and epididymis weights (compared with controls), differential morphology and histopathology, and altered sperm counts. In general, treatment was associated with reduced sperm counts and depressed sperm activity, with some histopathologic changes evident in the reproductive organs of younger animals. Comparative changes in testicular and epididymal weights, sperm count, motility, and viability were evaluated, along with the fertility and copulation indices of treated groups. Large reductions in testicular (>50%) and epididymal weights, sperm count, and motility were observed in those animals exposed to nitrobenzene for 14 days, while sperm viability and the fertility index were severely reduced in those males exposed to nitrobenzene for 21 days or more. While the copulation indices of treated males appeared unchanged with duration of exposure, the numbers of virgin females becoming pregnant by treated males declined markedly with duration of exposure. No mating females became pregnant in groups that were mated with males treated for 28 days or longer, an effect that appeared to result from the production of sperm with poor motility and reduced viability.
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