Toxicity of p-chloroaniline in rats and mice

Chhabra, Rajendra S.; Thompson, Miles D.; Elwell, Michael R.; Gerken, Diane K.

doi:10.1016/0278-6915(90)90148-g

Cited by 58 publications

(32 citation statements)

References 11 publications

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“…The primary target of aniline insult in rats appears to be the hemopoietic system, and injury is characterized by methemoglobinemia, hemolysis, and hemolytic anemia (Harrison & Jollow, 1986;Kim & Carlson, 1986;Khan et al, 1993Khan et al, , 1995 and by the development of hyperplasia, siderosis, and a variety of sarcomas of the spleen on prolonged exposure (Bus & Popp, 1987). Many of the characteristics of splenic toxicity in rats such as splenomegaly, hyperplasia, hyperpigmentation, and/or formation of highly malignant tumors (e.g., fibrosarcomas) are not restricted to aniline but also occur when animals are fed with substituted anilines such as o-toluidine (Goodman et al, 1984), chloroaniline (Ward et al, 1980;Chhabra et al, 1990), p-nitroaniline (Nair et al, 1990), 4,4'-sulfonyldianiline (Goodman et al, 1984), D&C red dye no. 9 (Weinberger et al, 1985) and substituted phenylurea herbicides (Wang et al, 1993).…”

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Erythrocyte‐aniune interaction leads to their accumulation and iron deposition in rat spleen

Khan

Kaphalia

Ansari

1995

Journal of Toxicology and Environmental Health

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In order to understand the splenic toxicity of aniline in rats, early interaction of aniline with erythrocytes and its subsequent deposition and covalent binding to macromolecules in target (spleen) and nontarget (liver) organs have been studied. Male Sprague-Dawley (SD) rats were given 1 or 3 doses of 1 mmol/kg [14C]aniline hydrochloride (1 dose/d) by gavage and euthanized 24 h after the treatment. Among blood components, maximum radioactivity was found to be associated with red blood cells (RBCs). After 3 doses, there was 112, 79, and 67% increase in the radioactivity in the whole blood, RBCs, and hemolysate, respectively, in comparison to 1 dose. In comparison to RBCs, plasma had only 40 and 16% radioactivity after the administration of 1 and 3 doses, respectively. Spleen homogenate at 1 dose had one-third of the radioactivity in the TCA precipitate, which increased to 40% at 3 doses, while the total radioactivity increased 256% over 1 dose. Liver, which had almost double the radioactivity on a per gram tissue basis compared to the spleen at one dose, did not show any appreciable increase in the radioactivity at three doses. However, radioactivity in the TCA precipitate of liver homogenate increased by 92% after 3 doses. The iron content of the spleen in rats given 3 doses of [14C]aniline increased by 85% compared to the rats given just 1 dose. The iron content of liver did not show any change at three doses. These data thus demonstrate a dose-dependent binding and accumulation of radioactivity in erythrocytes and spleen. These interactions, along with parallel increases in the iron content of the spleen, could be critical in the splenic toxicity of anilines.

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Erythrocyte‐aniune interaction leads to their accumulation and iron deposition in rat spleen

Khan

Kaphalia

Ansari

1995

Journal of Toxicology and Environmental Health

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“…Aniline and ring-substituted anilines are toxic, recalcitrant, and major products of herbicide metabolism in the soil (12,23). They have been reported to exhibit significant mammalian toxicity (14,58) and acute toxic effects on fish (25); thus, they are considered important environmental pollutants (38). Although anilines are decomposed by a variety of physicochemical processes such as evaporation, autooxidation, photooxidation, and chemical binding (see the references in reference 34), Lyons et al (34) have reported that the major pathway for their removal from aquatic environments is through biodegradation.…”

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Nucleotide sequences and regulational analysis of genes involved in conversion of aniline to catechol in Pseudomonas putida UCC22(pTDN1)

1997

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“…Many of the characteristics of splenotoxicity in rats, such as hyperplasia, hyperpigmentation, and/or formation of highly malignant tumors such as fibrosarcomas, are not restricted to aniline exposure, but also occur when animals are exposed to substituted anilines such as chloroaniline (Ward et al, 1980;Chhabra et al, 1990), p-nitroaniline (Nair et ai, 1990), o-toluidine (Goodman et al, 1984), 4,4'-sulfonyldianiline (Goodman et al, 1984), D&C red dye No. 9 (Weinberger et al, 1985), and substituted phenylurea herbicides (Wang et al, 1993).…”

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Oxidative Stress in the Splenotoxicity of Aniline

Khan

Boor

et al. 1997

Toxicol Sci

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Aniline-induced splenic toxicity is characterized by hemorrhage, capsular hyperplasia, fibrosis, and a variety of sarcomas in rats. Early biochemical events responsible for the observed effects are not known. To understand the mechanism(s) of aniline-induced splenic toxicity, single and multiple (four and seven) doses of 1 mmol/kg of aniline hydrochloride(AH) were given in rats. Apart from changes in the hematological parameters, these studies demonstrated that AH could induce lipid peroxidation and protein oxidation in the spleen, and significant increases were observed at four doses. Subsequently, a dose-response study of AH was performed. Male SD rats were given four doses each (one dose/ day) of 0.25, 0.5, 1, and 2 mmol/kg of AH in water by gavage, while controls received water only. Animals were euthanized 24 hr following the last dose and tissues obtained. Spleen weight increased by 32 and 80% at 1 and 2 mmol/kg doses, respectively. Splenic lipid peroxidation showed dose-dependent increases of 24, 32, and 43% at 0.5, 1, and 2 mmol/kg, respectively. Protein oxidation in the spleen, quantitated by carbonyl content per milligram protein, showed 10, 28, and 27% increases at 0.5, 1, and 2 mmol/ kg, respectively. Iron content in the spleen also showed dose-dependent increases of 72, 172, and 325% at 0.5, 1, and 2 mmol/kg, respectively. Dose-related histopathologic expansion of splenic red pulp was characterized by increasing vascular congestion (most pronounced at 2 mmol/kg), increased red pulp cellularity, erythrophagocytosis, and cellular fragmentation at 1 and 2 mmol/kg; iron deposition in red pulp also increased dramatically with dose. These studies establish that aniline induces lipid peroxidation and protein oxidation in the spleen and suggest that oxidative stress plays a role in the splenic toxicity of aniline, e 1997 society of Toxicology.

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Toxicity of p-chloroaniline in rats and mice

Cited by 58 publications

References 11 publications

Erythrocyte‐aniune interaction leads to their accumulation and iron deposition in rat spleen

Erythrocyte‐aniune interaction leads to their accumulation and iron deposition in rat spleen

Nucleotide sequences and regulational analysis of genes involved in conversion of aniline to catechol in Pseudomonas putida UCC22(pTDN1)

Oxidative Stress in the Splenotoxicity of Aniline

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