Renal and hepatic histopathology of intraperitoneally administered potassium permanganate on Clarias gariepinus juveniles

The biochemistry and histopathology of intraperitoneally administered potassium permanganate was investigated in Clarias gariepinus. Acute toxicity of the KMnO4 was determined by intraperitoneally injecting the fish with 0.0, 1.5, 2.0, 4.0 and 6.0 mg/kg. The 96 h lethal concentration (LC50) value obtained from the intraperitoneal injection of the juveniles of C. gariepinus with KMnO4 was 2.001 mg/kg KMnO4 at 95% confidence limit. Liver and kidney were excised at the end of each interval of exposure of 0 to 15 days and blood samples were obtained at the end of the exposure period from the caudal ablation and were used for the assay of creatinine, urea and blood urea nitrogen (BUN). The mean creatinine and BUN values differed significantly at P<0.05 when compared with the mean values of the control group at the same time. The KMnO4 caused histopathological changes and distortions in the histoarchitecture of the kidney (such as necrotic tubules, cystic spaces, and destruction of renal tubules) and the liver (such as disintegration of hepatic chords, enlargement of the sinusoids, and liver steatosis) of the fish. The potassium permanganate widely used in controlling external fungal, bacterial and protozoan infections of fish should not be indiscriminately used.


INTRODUCTION
Potassium permanganate is a strong oxidant, because of its derivative permanganate ion, MnO -2 (Šišperová et al., 2015).It is used as a common biocide at recommended concentrations up to 4 mg/L in various aquaculture setups (kori-Siakpere et al., 2011).Currently, KMnO 4 is a U.S Food and Drug Administration (FDA) investigational new animal drugs (INAD) under investigation by Carus Chemical Company Peru.The toxicity margin of KMnO 4 is narrow (1 to 3 mg/L) (Plumb, 1999).Toxicity levels have been determined for carp fry as an LC 50 ranging from 37.5 to 48 mg/L at 26°C and 45 to 37.5 mg/L at 32°C, at 24 and 48 h, respectively (Plumb, 1999;Ezemonye and Ogbomida, 2010).A limited amount of information is available about the toxicity of KMnO 4 .The acute toxicity of KMnO 4 to various fish species has been studied (Markings and Bills, 1975;Tucker, 1987).
These include several studies investigating striped bass and the hybrid striped bass (Straus, 2004) and Clarias gariepinus Juveniles (Kori-Siakpere, 2008, 2009).Potassium permanganate is poisonous when taken into the blood (Martin, 2003).It consists of dark, odorless, purple crystals with a metallic luster which are soluble in water giving pink to deep purple solutions depending on concentrations (Abalaka, 2013).It is a water disinfectant (Wells, Ponds) and is used as a gastric lavage in alkaloidae poisoning, but promotes rusting.It is an effective algicide (0.01%) and virucide (1%), but concentrations > 1:10,000 tend to irritate tissues (Khan, 2005).Hence, it may contaminate water and can be toxic without prodromal signs; the main lesions are hemorrhage and necrosis of crops in birds.Since potassium permanganate is still used chemically, there is need to access the toxicity of the compound (Brander and Bywater, 1992).The impact of contaminants on the aquatic ecosystem can be measured through a variety of parameters, from low levels of biological organization (molecular and biochemical responses) to high organization levels (population and community responses).In this context, the use of biomarkers at cellular and pathological levels is extremely important as a sensitive tool to measure the biological effect during the assessment of environmental quality, since they are more specific, sensitive, reproducible, and easy to determine.There is no pattern or established limit to this compound and it may be used freely and without restriction in aquaculture.According to the Food and Drug Administration (FDA), the inclusion of this compound in a regulatory class still depends on further studies.Several studies on the implementation and effectiveness of potassium permanganate in aquaculture are available in the literature, but information about its toxic potential in organs and tissues when intraperitoneally injected in fish is still scanty.The impact of contaminants on the aquatic ecosystem can be measured through low levels of biological organization (molecular, biochemical and histopathology) to high levels (community and population response) (FAO, 2010).In this context, histopathology and biomarkers are used as sensitive tools to measure the biological effects during the assessment of environmental quality, since they are more specific, sensitive, reproducible and easy to determine.The general objectives of the study were to determine the LC 50 of intraperitoneally administered potassium permanganate on C. gariepinus juveniles, ascertain the histopathological, and biochemical alterations in the liver and kidney in C. gariepinus Juveniles intraperitoneally administered with potassium permanganate.

Procurement of the experimental fish
The juveniles of C. gariepinus of average weight 23.4 ± 6.9 g were used in this experiment.The fish were obtained from a commercial fish farmer (Freedom Fisheries) at Enugu.They were transported to the Department of Zoology and Environmental Biology, University of Nigeria, Nsukka.Thereafter, they were kept in a well aerated chlorine free tap water at 25°C and acclimated for two weeks in the laboratory before the commencement of the study.The fish was fed with Coppens fish feed containing 55% crude protein and the water quality was maintained daily with a standard test kit.

Collection of the test compound and preparation of stock solution
The test compound, potassium permanganate used in this study was of analytical grade with 99.97% purity and was purchased from Ogige Market, Nsukka, Enugu State, Nigeria.The stock solutions were obtained and serial dilutions were made.

Acute toxicity bioassay and behavioural responses
Acute toxicity bioassay to determine the 96 h LC50 values of potassium permanganate was conducted using the standard protocols (APHA, AWWA, WPCF, 2005).The range finding test was carried out prior to determine the concentrations of the test chemical for the definitive test.For the definitive test, 150 fish of mean weight 14.71 ± 13.61 g were randomly distributed into five groups (A to E) and each group was replicated into three with ten fish per replicate and each fish was intraperitoneally injected with 1.5, 0.4002, 4.0, and 6.0 mg/kg.The experiment was set to determine the LC50 values of the test chemical.Fish were visually examined daily and considered dead when no sudden swimming in response to gentle touch was observed.Dead fish were removed with plastic forceps and the mortality was recorded at intervals of 24, 48, 72, and 96 h.The LC10-90 values of the test compound (KMnO4) for the fish at 24, 48, 72, and 96 h was determined by probit analysis (Finney, 1971).The behavioural responses of C. gariepinus at different concentrations of KMnO4 were observed from 24 to 96 h of the injection.

Sub lethal test
The 96 h LD50 value of KMnO4 in the present study was determined to be 2.001 mg/kg.Based on this value, three sub lethal concentrations of 0.1001, 0.2001 and 0.4002 mg/kg corresponding to 1/20, 1/10 and 1/5th of KMnO4, respectively were prepared by serial dilution of the stock solution.A total of thirty acclimatized fish were injected with each of the aforementioned sub lethal concentrations in triplicates of ten fish per replicate.Another set of 30 fish were injected intraperitoneally with 0.20 normal saline and were considered as the normal saline control groups.Control fish specimens were maintained in dechlorinated tap water without intraperitoneal injection with KMnO4 or normal saline.The experiment lasted for 15 days and the liver and kidney of the test fish were excised at intervals of five days and taken for analysis.

Water quality analysis
The water quality parameters (temperatures, pH and dissolved oxygen) of experimental set up with KMnO4 toxicant and control bioassay were monitored by the procedure according to APHA (1998).Before the commencement of the study, the water temperature was 25.5°C, pH 6.5 and dissolved oxygen 5.2 mg/L.The behavioural responses of the fish were noted, such as erratic swimming and gasping of air.

Biochemicals
Blood samples were taken on the fifteenth day of administration of KMnO4.Blood samples were taken in tubes and centrifuged at 3000 rpm for 10 min for serum separation.The serum was stored at -20 o C for further analysis.

Determination of creatinine
Calibration graph for the estimation of creatinine was carried out in a 3 ml reagent mixture containing 1.93 mM metol, 68.8 µM copper and 1 mM acetic acid/sodium acetate buffer of pH 5.4.The reaction was initiated by adding 100 µl of creatinine concentrations.The reaction mixture was allowed to stand for 30 min at room temperature.Absorbance was read at 530 nm (Copper and Bigga, 1961).

Determination of serum urea
This was carried out using Randox kit for serum urea estimation, following the experimental procedures described by the manufacturer.The absorbance was spectrophotometrically read at 546 nm and calculations were made thus; Urea concentration (mg/dl) = A sample / A standard × standard concentration.

Histopathology
The tissue samples liver and kidney were quickly excised from the fish and fixed in bouins fluid.Slices of the organs were quickly prepared for histological examination to show if there were morphological changes in the organs during the treatment.Processing started by parking the tissue in the tissue capsule.The tissues were dehydrated in graded level of ethanol (70 to 100%) in ascending order.Alcohol was changed after soaking the tissue in them for 1 to 2 h.The tissue was cleaned in chloroform and impregnated with paraffin wax and sectioned at 4 to 5 micron thickness.The section was floated on a water bath maintained at 2 to 3°C below the melting point of paraffin wax.They were dried between 15 and 30 min and were stained with haematoxylin and eosin (H&E), dehydrated, cleaned and mounted (DCM) in a mountant, avoiding air bubbles.Photomicrograph was taken using motic camera with ×40 and ×10 objectives.

Statistical analysis
Mean values were analyzed for significant differences (P < 0.05) using the analysis of variance (ANOVA).Differences between means were partitioned using the Duncan new multiple range test.Statistical Package for Social Sciences (SPSS) version 16 was used.Probit value was determined from the probit model developed by Finney (1959).

Water quality parameters
Before the commencement of the study, the water temperature was 25.5°C, pH 6.5 and dissolved oxygen 5.2 mg/L.

Lethal concentration (LC 50 ) determination
The mortality of C. gariepinus injected with different concentrations of potassium permanganate is shown in Table 1.A dose-dependent increase and a time dependent decrease was observed in the mortality rate, such that as the exposure time increases from 24 to 96 h, the lethal concentration required to kill the fish was reduced.From the results obtained in the acute toxicity bioassay, a total percentage mortality of 20, 60, 90 and 100% were observed at the end of 24, 48, 72 and 96 h, respectively.A probit analysis was carried out with the result shown in Table 1 and LC 50 value of 2.001 mg/kg was obtained.

Behavioural responses of C. gariepinus intraperitoneally administered with KMnO 4
The results showed that potassium permanganate affected the behavioural characteristics of C. gariepinus.The control specimens were not hyperactive and showed normal swimming patterns and fin movements throughout the exposure period.The normal saline control groups showed some degree of hyperactivity and jerky movements.However, with increasing KMnO 4 concentrations and exposure duration time, hyperactivity and jerky movements increased.In contrast, the swimming rate, fin movement and equilibrium status decreased as shown in Table 2.

Changes in the degree of lesions (wounds, cm) in the skin of C. gariepinus Juveniles intraperitoneally administered with various concentrations of KMnO 4
The effect of the increasing concentration of intraperitoneally administered KMnO 4 after 15 days treatment produced a duration dependent significant (p < 0.05) increase in the lesion (wound) levels in the skin of C. gariepinus Juveniles.Table 3 shows the degree of lesions (wounds) in cm observed during intraperitoneal injection with KMnO 4 .A one way ANOVA was used to analyze the lesion degrees shown in Table 3 and the differences between means were partitioned using the Duncan multiple range test with SPSS version 16; the mean values observed in Table 4 was thus obtained.Actually, group B administered with 0.1001 mg of KMnO 4 had the highest degree of lesion, followed by group C (0.2001 mg KMnO 4 ) and group D (0.4002 mg KMnO 4 ).When compared with the normal saline, control group A was administered with normal saline only.The increase in lesions was time and concentration dependent as shown in Table 3. Lesions did not occur in the control treated groups differed significantly at P < 0.05 when compared with the control.The decrease in the creatinine, urea and BUN among the treated groups had concentration independent changes at the end of the exposure period (Table 5).

Juveniles intraperitoneally administered with KMnO 4
Histopathological changes observed in the kidney (Table 6) of C. gariepinus intraperitoneally administered with KMnO 4 showed that the kidney of the control group (normal) exhibited intact tubules (Plate 1); however, the group administered with 0.2 mg/kg of normal saline showed necrotic tubules, and destruction of tubules (Plate 2) intact and severe degeneration of tubules as well as intact sinusoids and vacuolations, Plate 3 and cyctic spaces (Plate 4) were seen in days 5 and 15; therefore, the kidney in group B administered with 0.1001 mg/kg KMnO 4 showed partial destruction of renal tubules (Plate 5) in day 5, whereas atrophy of the proximal and distal convoluted tubules and massive cystic spaces where evident (Plate 6) in day 10.Meanwhile, in day 15, the kidney architecture appeared normal with tubules being intact without any structural damages as shown in Plate 6.However, group C treated with 0.2001 mg/kg of KMnO 4 exhibited increase proliferation of polymorphonuclear cells especially in day 10 (Plate 7),

Group Day 5 Day 10
Day 15 A ---B 0.3, 0.4, 0.3 cm 1.0, 1.3, 0.5 cm 2.5, 1.5, 1.7 cm C 0, 0, 0 cm 0.9, 1.0, 0.4 cm 2.0, 1.2, 1.5 cm D 0, 0, 0 cm 0.9, 1.0, 0 cm 1.8, 1.0, 1.2 cm     The histopathological changes in the C. gariepinus Juveniles intraperitoneally administered with KMnO 4 showed varied degrees of structural changes in the liver (Table 7).The control liver showed intact parenchymal cells, central vein and sinusoids which usually keeps for the normal structural features seen in the liver (Plate 10); meanwhile, throughout the exposure period especially in the group administered with 0.2 mg/kg of normal saline showed disintegration of hepatic chords Plate 11 which lead to the multiple dilation/or enlargement of the sinusoids (Plate 12) at day 15, whereas, at day 5 no histopathological changes was observed.In addition, there is an onset of liver steatosis due to the visible accumulation of varied sizes of fat droplets (Plate 13) most especially in the group administered with 0.1001 mg/kg KMnO 4 in day 10, but in day 15, there was no observable changes in the liver of the fish.Similar fatty  At the highest dose administered to group D (0.4002 mg/kg), the liver tissue showed multiple hyperemias at the end of day 10 exposures (Plate 17) and in day 15, there was a disintegration of hepatic chords (Plate 18).

DISCUSSION
Intraperitoneal administration of KMnO 4 to fish inflicts Plate 12. Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.2 mg/kg of normal saline after 10 days, showed distorted hepatic chords with dilatation of sinusoids (double head black arrow).However, small bile duct (star) is evident and at the same time, hepatic lobes (red star) can be seen with minor blood congestion (black arrow) in between lobes.H&E, magnification x100.
stresses on the mechanisms required to maintain a healthy physiological state.These stresses lead to behavioural changes, and changes in their biochemical and physiological processes.In view of this, there has been increasing interests in examining the physiological, biochemical and histopathological stress responses in aquatic vertebrates to protect aquatic life.The physicochemical parameters of the test were slightly similar during the toxicity test.The percentage mortality observed in the acute study was shown to increase with increasing doses of the intraperitoneally administered KMnO 4 .The observation is in consonance with earlier report of Kori-Siakpere (2008).Kori-Siakpere (2008) further reported that the level of any pesticide depends on it bio-accumulation, the different chemistries of the compounds forming the pesticides and the reactions of the organisms receiving the toxicant.The value obtained from the toxicity test in this study agrees with the report of Kori-Siakpere (2008).The water quality parameters may have possibly contributed to the variations in the behavioural pattern and the mortality of the test fish during the study period.During the acute toxicity study, C. gariepinus Juveniles were stressed progressively leading to possible observable behavioural changes such as erratic swimming or less of reflex, etc., with time before death.The stressful behavior of respiratory impairment due to the toxic effect of KMnO 4 particularly on the gills may have impaired the respiratory organ.Death could therefore have occurred either by direct poisoning or indirectly by making the medium unconducive or even by both, whichever is the case, the source of death was potassium permanganate.This demonstrates the observations of Ayoola (2008), that in all toxicants, a threshold is reached above which there is no drastic survival of the animal.Below the threshold, the animal is in a tolerance zone of resistance.The time of toxicity disappearance and mortality were observed from the record of relative mortality time in different concentration of potassium permanganate for 96 h.The creatinine and urea test has commonly been used to diagnose impaired kidney function and to detect renal damage.However, in the present experiment, there was significant difference in serum creatinine levels in the intraperitoneally administered KMnO 4 in C. gariepinus Juveniles when compared with the control group.These findings had shown that creatinine may be an accurate biomarker to distinguish dysfunction in kidney tissues.Hence, urea and creatinine are widely used to access renal sufficiency.Higher than normal level of serum urea and creatinine are indications of deficiency in renal function.
Thus, the increase in serum urea concentrations with concomitant increase in serum creatinine concentration in the infected treated animals, suggest that the normal functioning of the kidney has been compromised.Increase in urea level depicts that KMnO 4 elicits the elevation.Moreover, the fairly increased levels of serum creatinine in the current study may be induced by glomerular insufficiency, increased muscle tissue catabolism or impairment of carbohydrate metabolism.Histopathological examination of the liver and the kidney of the exposed fish indicated that the kidney and the liver were affected.The liver is the main organ for detoxification (Dutta et al., 1993;Abalaka, 2013).The teleost liver is one of the most sensitive organs with regards to showing alterations in histoarchitecture, biochemistry and physiology following exposure to various types of environmental conditions (Rodrigues and Fanta, 1998).Moreover, in the liver sections of the normal fish, the hepatocytes form a rather cord-like pattern.These cords are arranged around tributaries of the hepatic vein.The liver cells are intact, polygonal in shape with homogenous eosinophilic cytoplasm and centrally located nuclei.Large number of sinusoids appeared intact and slightly separates the cords from another.
The histopathologIcal changes in the liver were more pronounced in days 5, 10 and 15, but the degree of damages varied according to the dosages of KMnO 4 administered.The present result showed that KMnO 4 induced many histopathological changes in the liver of the catfish C. gariepinus.These changes include distorted hepatic chords that led to massive increase in the sinusoids which is usually characterized by widening of hepatic capillaries which may involve the entire lobule or predominantly in the central, periportal or medial areas which can be encountered in different situations.These changes were mainly evident among the groups treated with 0.2 mg/kg normal saline, and 0.1001 mg/kg KMnO 4 at the 5th day of exposure.Further, the blood congestion observed in the liver of the test fish in the group treated with 0.2 mg/kg of normal saline in day 10 may be due to the fact that the central vein and sinusoids distended with red blood cells (RBCs) and some areas of hemorrhage are present when RBCs are phagocytized by macrophages.At the same time, these sinusoids clog up thereby blocking the blood from the hepatic artery and interbillary portal vein which have to pass through the sinusoids to get to the central vein.The fatty accumulation in the liver tissues seen as lipid droplets observed among the groups treated with 0.1001 and 0.2001 mg/kg at days 5 and 10, respectively, may be due to abnormal retention of lipids accumulated in the vesicles (a small organelle within a cell consisting of fluid) that displace cytoplasm when the vesicles are large enough to distort the nucleus.This is keeping for the fact that the liver is the primary organ of lipid metabolism which is most associated with steatosis.This also agrees with Sakr and Gabar (1991) who reported fatty degeneration among large number of cells in C. gariepinus exposed to fenvelarte.Desai et al. (1984) reported vacuolation of hepatocytes, fatty degeneration and necrosis in Tilapia mossanbica exposed to monocrotophos.There is still paucity of literature on the toxicity of intraperitoneally administered KMnO 4 in fishes, especially towards histopathological alterations.
Kidney is the functional unit composed of nephrons.Each nephron is made up of a renal cortex and well developed renal tubules.The kidney of C. gariepinus juveniles exposed to KMnO 4 showed tubular destruction or fusion of tubules, cystic spaces and necrotic tubules.Renal corpuscles of the kidney were scattered resulting in the disorganization and consequently obstruction to their physiological functions.
These findings agree with the report of Omotoyin et al. (2006).Lesions in the kidney of fish exposed to deltamethrin in the epithelial cells of the renal tubule, pyknotic nuclei in the hematopoeitic tissues, degeneration of glomerulus were observed (Elif, 2006).Whereas, some of the groups especially the group treated with 0.1001 and 0.2001 mg/kg of KMnO 4 at days 5 and 10, respectively maintained intact tubules with intact brush border cells.The destruction or degeneration of tubules observed in the present work may be due to autolytic action of lysosomal enzymes released out of these organelles to the ground cytoplasm or due to reabsorption of excreted protein molecules which are generally represented in the glomerular filtrate.More so, it appears that the kidney's tubular cell may possess a transport mechanism similar to that of the hepatocyte (the multi-specific bile acid transport system) which is responsible for the uptake of the chemical (KMnO 4 ) into the cell.

Conclusion
The results of this study have demonstrated that the use of concentrations considered safe by literature for prophylaxis and treatment of diseases in fish farming (0.1001, 0.2001 and 0.4002 mg/kg KMnO 4 ) may cause considerable changes to the health of exposed fish, thus evidencing the toxic potential of KMnO 4 in non target organisms.Such alterations in the histopathology and biochemical markers have pointed out that potassium permanganate can be toxic; therefore, the use of different biomarkers become important as they can reflect more accurately the toxicity of contaminant substances studied and their effects impacting the aquatic ecosystem.It is hereby recommended that KMnO 4 widely used in controlling external fungal, bacterial and protozoan infections of fish should not be used indiscriminatingly.
same alphabets along the column are not statistically significant.Means with different alphabets along the column are statistically significant at P < 0.05.
, 1: mild, 2: moderate, 3: strong.Plate 11.Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.2 mg/kg of normal saline after 5 days, showed intact hepatocytes (cirles).H&E, magnification x100.accumulation (macro and micro vesicular) were also observed in the day 5 of the group administered with 0.2001 mg/kg KMnO 4 (Plate 14), while in day 10, the liver appeared to be normal without any visible changes in the architecture as shown in Plate 15.The degree of cytoplasmic vacuolation of hepatocytes and massive inflammatory cells were evident in day 15 in the same group administered with 0.2001 mg/kg KMnO 4 (Plate 16).

Plate 13 .
Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.1001 mg/kg of KMnO4 after 5 days, showed dilatated sinusoids.H&E, magnification x100.Plate 14. Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.1001 mg/kg of KMnO4 after 10 days, liver showed fat accumulation as lipid droplets (micro and macro vesicular fatty change) which usually appears to be consistent with vacuolation of glycogen content.Plate 15.Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.2001 mg/kg of KMnO4 after 10 days, showed intact liver architecture with sinusoids and hepatocytes.H&E, magnification x100.

Plate 16 .
Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.2001 mg/kg of KMnO4 after 15 days, tissue showed central vein with infilteration of inflammatory cells (black arrow), traces of bile pigments (red arrow) evident and cytoplasmic vacuolation of heptocytes.H&E, magnification x100.Plate 17. Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.4002 mg/kg of KMnO4 after 10 days, showed hyperemia (black arrow).H&E, magnification x100.Plate 18. Photomicrograph of C. gariepinus liver intraperitoneally administered with 0.4002 mg/kg of KMnO4 after 15 days, showed minor disintegration of hepatic chords (black arrow) evident which led to sinusoid enlargement.H&E, magnification x100.The black stains in the photomicrograph are formalin pigments which can be called artifacts.

Table 1 .
Summary of mortalities in C. gariepinus juveniles intraperitoneally administered with KMnO4.

Changes in some biochemical markers in C. gariepinus intraperitoneally administered with KMnO 4 at the end of the exposure period
Similarly, the changes in the normal BUN in the KMnO 4 treated groups showed that group B treated with 1.5 mg/kg of KMnO 4 had the highest BUN value of 19.31 + 0.96, followed by group A (0.1001 mg/kg) with BUN value of 15.06 + 0.64 and group C (0.4002 mg/kg KMnO 4 ) with BUN value of 11.69 + 0.64.The BUN values among the KMnO 4 Moreover, the control groups treated with normal saline maintained urea level of 27.44 ± 3.51 mg/dl.

Table 2 .
Behavioural changes of Clarias gariepinus intraperitoneally administered with various concentrations of KMnO4.

Table 3 .
Various degrees of lesions (wounds) in cm observed in the skin of C. gariepinus intraperitoneally administered with normal saline and various concentrations of KMnO4.

Table 4 .
Changes in the degree of lesions (cm) in the skin of C. gariepinus intraperitoneally administered with KMnO4.

Table 5 .
Changes in some biochemical markers in C. gariepinus intraperitoneally administered with KMnO4 at the end of the exposure period (15 days).
whereas at the end of the treatment, the kidney of the C. gariepinus administered with 0.2001 mg/kg KMnO 4 appeared to have intact kidney architecture especially at renal cortex of the kidney as shown in Plate 8.Furthermore, group D administered with 0.4002 mg/kg of KMnO 4 had no pathological changes in days 5 and 15,

Table 6 .
Summarized histopathological effects in the kidney of C. gareipinus intraperitoneally administered with KMnO4.

Table 7 .
Summarized histopathological effects in the liver of C. gareipinus intraperitoneally administered with KMnO4.